BUFFALO, NY- December 20, 2023 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 23, entitled, “Benidipine calcium channel blocker promotes the death of cigarette smoke-induced senescent cells and improves lung emphysema.” Smoking is the main risk factor for many lung diseases including chronic obstructive pulmonary disease. Cigarette smoke (CS) contains carcinogenic and reactive oxygen species that favor DNA mutations and perturb the homeostasis and environment of cells. CS induces lung cell senescence resulting in a stable proliferation arrest and a senescence-associated secretory phenotype. It was recently reported that senescent cell accumulation promotes several lung diseases. In this new study, researchers Alberta Palazzo, Gabriela Makulyte, Delphine Goerhig, Jean-Jacques Médard, Vincent Gros, François Trottein, Serge Adnot, David Vindrieux, Jean-Michel Flaman, and David Bernard from Université de Lyon, Equipe Labellisée la Ligue Contre le Cancer, Université Paris Est Créteil, Hôpital Henri Mondor, and Université Lille performed a chemical screen, using an FDA-approved drug library, to identify compounds selectively promoting the death of CS-induced senescent lung cells. “Here, our aim was to identify senolytic compounds in the context of CS-induced senescence and to assess whether they improved lung emphysema.” Aside from the well-known senolytic, ABT-263, the researchers identified other potentially new senescence-eliminating compounds, including a new class of molecules, the dihydropyridine family of calcium voltage-gated channel (CaV) blockers. Among these blockers, Benidipine decreased senescent lung cells and ameliorates lung emphysema in a mouse model. The dihydropyridine family of CaV blockers thus constitutes a new class of senolytics that could improve lung diseases. “Hence, our work paves the way for further studies on the senolytic activity of CaV blockers in different senescence contexts and age-related diseases.” DOI - https://doi.org/10.18632/aging.205259 Corresponding author - David Bernard - david.bernard@lyon.unicancer.fr Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205259 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, senolytic, cigarette smoke, lung disease, cellular senescence, calcium channel About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- December 19, 2023 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 23, entitled, “Sirtuin 6 activation rescues the age-related decline in DNA damage repair in primary human chondrocytes.” While advanced age is widely recognized as the greatest risk factor for osteoarthritis (OA), the biological mechanisms behind this connection remain unclear. Previous work has demonstrated that chondrocytes from older cadaveric donors have elevated levels of DNA damage as compared to chondrocytes from younger donors. In this new study, researchers Michaela E. Copp, Jacqueline Shine, Hannon L. Brown, Kirti R. Nimmala, Oliver B. Hansen, Susan Chubinskaya, John A. Collins, Richard F. Loeser, and Brian O. Diekman from University of North Carolina at Chapel Hill, North Carolina State University, Rush University Medical Center, and Thomas Jefferson University aimed to determine whether a decline in DNA repair efficiency is one explanation for the accumulation of DNA damage with age, and to quantify the improvement in repair with activation of Sirtuin 6 (SIRT6). “In this study, we use irradiation as an acute model of DNA damage to bring the level of damage to equivalent levels across chondrocytes from donors of various ages.” After acute damage with irradiation, DNA repair was shown to be more efficient in chondrocytes from young (≤45 years old) as compared to middle-aged (50–65 years old) or older (>70 years old) cadaveric donors. Activation of SIRT6 with MDL-800 improved the repair efficiency, while inhibition with EX-527 reduced the rate of repair and increased the percentage of cells that retain high levels of damage. In addition to affecting repair after acute damage, treating chondrocytes from older donors with MDL-800 for 48 hours significantly reduced the amount of baseline DNA damage. Chondrocytes isolated from the knees of mice between 4 months and 22 months of age revealed both an increase in DNA damage with aging, and a decrease in DNA damage following MDL-800 treatment. Lastly, treating murine cartilage explants with MDL-800 lowered the percentage of chondrocytes with high p16 promoter activity, which supports the concept that using SIRT6 activation to maintain low levels of DNA damage may prevent the initiation of senescence. “In conclusion, the findings presented here support the hypothesis that the efficiency of DNA damage repair declines with age in chondrocytes and that SIRT6 activation improves repair both in response to an acute irradiation challenge and in the context of age-related damage accumulation. These results emphasize the critical role of SIRT6 in DNA repair and support further studies investigating the use of MDL-800 (or alternative SIRT6 activators) in mitigating senescence induction and ameliorating OA development.” DOI - https://doi.org/10.18632/aging.205394 Corresponding author - Brian O. Diekman - bdiekman@email.unc.edu About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- December 15, 2023 – A new #researchpaper was #published on the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 23, entitled, “Uncovering a unique pathogenic mechanism of SARS-CoV-2 omicron variant: selective induction of cellular senescence.” SARS-CoV-2 variants are constantly emerging with a variety of changes in the conformation of the spike protein, resulting in alterations of virus entry mechanisms. Solely omicron variants use the endosomal clathrin-mediated entry. In this new study, researchers Franziska Hornung, Nilay Köse-Vogel, Claude Jourdan Le Saux, Antje Häder, Lea Herrmann, Luise Schulz, Lukáš Radosa, Thurid Lauf, Tim Sandhaus, Patrick Samson, Torsten Doenst, Daniel Wittschieber, Gita Mall, Bettina Löffler, and Stefanie Deinhardt-Emmer from Jena University, Leibniz Centre for Photonics in Infection Research (LPI), University of California San Francisco, Klinik für Herz- und Thoraxchirurgie, and University Hospital Bonn investigated the influence of defined altered spike formations to study their impact on premature cellular senescence. “In our study, in vitro infections of SARS-CoV-2 variants delta (B.1.617.2) and omicron (B.1.1.529) were analyzed by using human primary small alveolar epithelial cells and human ex vivo lung slices. We confirmed cellular senescence in human lungs of COVID-19 patients. Hence, global gene expression patterns of infected human primary alveolar epithelial cells were identified via mRNA sequencing.” Solely omicron variants of SARS-CoV-2 influenced the expression of cell cycle genes, highlighted by an increased p21 expression in human primary lung cells and human ex vivo lungs. Additionally, an upregulated senescence-associated secretory phenotype (SASP) was detected. Transcriptomic data indicate an increased gene expression of p16, and p38 in omicron-infected lung cells. Significant changes due to different SARS-CoV-2 infections in human primary alveolar epithelial cells with an overall impact on premature aging could be identified. A substantially different cellular response with an upregulation of cell cycle, inflammation- and integrin-associated pathways in omicron infected cells indicates premature cellular senescence. “This difference may be attributed to the distinct endocytic cell entry and intracellular pathways of the omicron variant when compared to the delta variant. The induction of cellular senescence in lung tissue following acute SARS-CoV-2 infection could potentially contribute to the reported cytokine storm and the development of long-COVID.” DOI - https://doi.org/10.18632/aging.205297 Corresponding author - Stefanie Deinhardt-Emmer - stefanie.deinhardt-emmer@med.uni-jena.de Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, SARS-CoV-2, variant of concern, cellular senescence, lung airway cells About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- December 13, 2023 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 22, entitled, “Nectandrin B significantly increases the lifespan of Drosophila - Nectandrin B for longevity.” Phytochemicals are increasingly recognized in the field of healthy aging as potential therapeutics against various aging-related diseases. Nutmeg, derived from the Myristica fragrans tree, is an example. Nutmeg has been extensively studied and proven to possess antioxidant properties that protect against aging and alleviate serious diseases such as cancer, heart disease, and liver disease. However, the specific active ingredient in nutmeg responsible for these health benefits has not been identified thus far. In this new study, researchers Ji-Seon Ahn, Nasir Uddin Mahbub, Sura Kim, Han-Byeol Kim, Jong-Soon Choi, Hea-Jong Chung, and Seong-Tshool Hong from Korea Basic Science Institute, Jeonbuk National University Medical School and Chung-Ang University present evidence that Nectandrin B (NecB), a bioactive lignan compound isolated from nutmeg, significantly extended the lifespan of the fruit fly Drosophila melanogaster by as much as 42.6% compared to the control group. “[...] we hypothesized that NecB might possess anti-aging efficacy.” The dramatic reduction of intracellular ROS levels by NecB captured the researchers’ attention. NecB also improved age-related symptoms including locomotive deterioration, body weight gain, eye degeneration, and neurodegeneration in aging D. melanogaster. The researchers wrote that this result represents the most substantial improvement in lifespan observed in animal experiments to date, suggesting that NecB may hold promise as a potential therapeutic agent for promoting longevity and addressing age-related degeneration. “We strongly believe that NecB urgently needs further attention and research, as we believe it has made a potential contribution to our understanding of the aging process as well as its application as a potential therapeutic agent for longevity and age-related.” DOI - https://doi.org/10.18632/aging.205234 Corresponding authors - Jong-Soon Choi - jschoi@kbsi.re.kr, Hea-Jong Chung - hjchung84@kbsi.re.kr, and Seong-Tshool Hong - seonghong@jbnu.ac.kr Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205234 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, Myristica fragrans, nutmeg, Nectandrin B, lifespan, longevity About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- December 12, 2023 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 22, entitled, “Tat-heat shock protein 10 ameliorates age-related phenotypes by facilitating neuronal plasticity and reducing age-related genes in the hippocampus.” In this new study, researchers Hyo Young Jung, Hyun Jung Kwon, Kyu Ri Hahn, Woosuk Kim, Dae Young Yoo, Yeo Sung Yoon, Dae Won Kim, and In Koo Hwang from Seoul National University, Chungnam National University, Gangneung-Wonju National University, Hallym University, and Konkuk University investigated the effects of heat shock protein 10 (HSP10) protein on memory function, hippocampal neurogenesis, and other related genes/proteins in adult and aged mice. “In the present study, we investigated the effects of HSP10 on hippocampal function in both adult and aged mice.” To translocate the HSP10 protein into the hippocampus, the Tat-HSP10 fusion protein was synthesized, and Tat-HSP10, not HSP10, was successfully delivered into the hippocampus based on immunohistochemistry and western blotting. Tat-HSP10 (0.5 or 2.0 mg/kg) or HSP10 (control protein, 2.0 mg/kg) was administered daily to 3- and 21-month-old mice for 3 months, and observed the senescence maker P16 was significantly increased in aged mice and the treatment with Tat-HSP10 significantly decreased P16 expression in the hippocampus of aged mice. In novel object recognition and Morris water maze tests, aged mice demonstrated decreases in exploratory preferences, exploration time, distance moved, number of object contacts, and escape latency compared to adult mice. Treatment with Tat-HSP10 significantly improved exploratory preferences, the number of object contacts, and the time spent swimming in the target quadrant in aged mice but not adults. Administration of Tat-HSP10 increased the number of proliferating cells and differentiated neuroblasts in the dentate gyrus of adult and aged mice compared to controls, as determined by immunohistochemical staining for Ki67 and doublecortin, respectively. Additionally, Tat-HSP10 treatment significantly mitigated the reduction in sirtuin 1 mRNA level, N-methyl-D-aspartate receptor 1, and postsynaptic density 95 protein levels in the hippocampus of aged mice. In contrast, Tat-HSP10 treatment significantly increased sirtuin 3 protein levels in both adult and aged mouse hippocampus. These suggest that Tat-HSP10 can potentially reduce hippocampus-related aging phenotypes. “Our results suggest that Tat-HSP10 treatment facilitates mitochondrial function, and Tat-HSP10 supplementation ameliorates the aging phenotypes in the mouse hippocampus.” DOI - https://doi.org/10.18632/aging.205182 Corresponding authors - Dae Won Kim - kimdw@gwnu.ac.kr, and In Koo Hwang - vetmed2@snu.ac.kr Keywords - aging, heat shock protein 10, hippocampus, memory, neurogenesis, synaptic plasticity About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by deficits in communication and social interaction, as well as repetitive behaviors. It has been observed that children born to older fathers have an increased risk of developing ASD and other neurodevelopmental disorders. This phenomenon suggests that paternal age may have an impact on the risk of ASD in offspring. Recent research has focused on understanding the potential mechanisms underlying the association between paternal age and ASD. One area of interest is the epigenome, specifically DNA methylation, which refers to the addition or removal of methyl groups to DNA molecules. DNA methylation can affect gene expression and play a role in various biological processes. In a new study, researchers Ramya Potabattula, Andreas Prell, Marcus Dittrich, Caroline Nava, Christel Depienne, Yosra Bejaoui, Nady El Hajj, Thomas Hahn, Martin Schorsch, and Thomas Haaf from Julius Maximilians University, Groupe Hospitalier Pitié-Salpêtrière, University Hospital Essen, Hamad Bin Khalifa University, and Fertility Center in Wiesbaden, Germany, explored the relationship between paternal age, DNA methylation of the BEGAIN gene, and the risk of ASD. The BEGAIN gene encodes a protein involved in protein-protein interactions at synapses, which are crucial for proper brain function. On November 28, 2023, their research paper was published in Aging’s Volume 15, Issue 22, entitled, "Effects of paternal and chronological age on BEGAIN methylation and its possible role in autism." Full blog - https://aging-us.org/2023/12/what-makes-children-of-older-fathers-at-increased-risk-of-autism/ Paper DOI - https://doi.org/10.18632/aging.205275 Corresponding author - Thomas Haaf - thomas.haaf@uni-wuerzburg.de Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205275 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, age and sex effect, autism spectrum disorder, BEGAIN, chronological aging, paternal age effect, sperm methylation About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- December 6, 2023 – A new #editorial paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 22, entitled, “Artificial intelligence for aging research in cancer drug development.” Aging is a multifactorial and complex process associated with various diseases, including cancer. In light of the growing aging population, the need for effective cancer treatments is more significant than ever. Artificial intelligence (AI) is playing an increasingly crucial role in aging research and cancer drug development in revealing the critical drivers of outcomes among a wide range of intrinsic and extrinsic factors. In recent years, the use of AI in aging research has been rapidly increasing, suggesting that AI-based analysis of healthcare data may enhance clinical care. In this new editorial, researchers Dorsa Shirini, Lawrence H. Schwartz and Laurent Dercle from Columbia University Medical Center provide an overview of the potential benefits as well as the technical caveats of adopting AI to help researchers identify new targets, develop more effective therapies, and accelerate the discovery process of drug development in the context of aging research. “In this review, we discuss how we could leverage AI technologies to consider a patient’s unique aging profile and tailor cancer treatment more precisely to the individual. This approach would help optimize treatment outcomes, minimize treatment-related risks, and improve the overall quality of care for patients, considering the complex interplay between aging and cancer treatment response.” DOI - https://doi.org/10.18632/aging.204914 Corresponding authors - Laurent Dercle - ld2752@cumc.columbia.edu Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204914 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, artificial intelligence, cancer research About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- December 5, 2023 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 22, entitled, “Contribution of membrane raft redox signalling to visfatin-induced inflammasome activation and podocyte injury.” The number of obese patients with end stage renal disease has increased significantly worldwide in the last few decades. Obesity results in an increased risk for chronic kidney diseases like diabetes and hypertension which consequently result in chronic kidney disease or even end-stage renal disease. However, the exact mechanism of how obesity increases the advancement of chronic kidney disease is still uncertain. Recently, researchers Saisudha Koka, Sreenidhi Surineni, Gurinder Bir Singh, and Krishna M. Boini from the University of Houston, Texas A&M University and the University of California Riverside have shown that adipokine visfatin-induced NLRP3 inflammasome activation contributes to podocyte injury. However, the molecular mechanisms of how visfatin induces the Nlrp3 inflammasome activation and podocyte damage is still unknown. The present study tested whether the membrane raft (MR) redox signaling pathway plays a central role in visfatin-induced NLRP3 inflammasomes formation and activation in podocytes. “In this study, it is proposed that visfatin induces the NLRP3 inflammasome activation in podocytes, leading to glomerular inflammatory injury in the kidney and the development of CKD, may be primarily driven by NADPH oxidase-mediated membrane raft redox signalling.” Upon visfatin stimulation, an aggregation of NADPH oxidase subunits, gp91phox and p47phox, was observed in the MR clusters, forming an MR redox signaling platform in podocytes. The formation of this signaling platform was blocked by prior treatment with MR disruptor MCD or NADPH oxidase inhibitor DPI. In addition, visfatin stimulation significantly increased the colocalization of Nlrp3 with Asc or Nlrp3 with caspase-1, IL-β production, cell permeability in podocytes compared to control cells. Pretreatment with MCD, DPI, WEHD significantly abolished the visfatin-induced colocalization of NLRP3 with Asc or NLRP3 with caspase-1, IL-1β production and cell permeability in podocytes. Furthermore, Immunofluorescence analysis demonstrated that visfatin treatment significantly decreased the podocin and nephrin expression (podocyte damage) and prior treatments with DPI, WEHD, MCD attenuated this visfatin-induced podocin and nephrin reduction. In conclusion, their results suggest that visfatin stimulates membrane raft clustering in the membrane of podocytes to form redox signaling platforms by aggregation and activation of NADPH oxidase subunits enhancing O2·− production, leading to NLRP3 inflammasome activation in podocytes and ultimate podocyte injury. “Through experiments conducted on cultured podocytes, we have demonstrated, for the first time that membrane raft-associated redox signalling is essential for the NLRP3 inflammasomes assembly and activation in response to visfatin, subsequently resulting in podocyte dysfunction and injury. These findings shed light on a novel mechanism underlying inflammasome activation and injury of podocytes triggered by visfatin.” DOI - https://doi.org/10.18632/aging.205243 Corresponding author - Krishna M. Boini - kmboini@uh.edu Video short - https://www.youtube.com/watch?v=cIzaHj31GBo Visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- November 30, 2023 – A new #researchpaper was #published on the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 22, entitled, “Chronological aging impacts abundance, function and microRNA content of extracellular vesicles produced by human epidermal keratinocytes.” The disturbance of intercellular communication is one of the hallmarks of aging. In their new study, researchers Taku Nedachi, Christelle Bonod, Julie Rorteau, Wafae Chinoune, Yuri Ishiuchi, Sandrine Hughes, Benjamin Gillet, Nicolas Bechetoille, Dominique Sigaudo-Roussel, and Jérôme Lamartine from the University of Lyon, Toyo University and Gattefossé SAS aimed to clarify the impact of chronological aging on extracellular vesicles (EVs), a key mode of communication in mammalian tissues. “The present study was therefore conducted to elucidate whether the characteristics of EVs released from cultured human keratinocytes can be modulated during aging process.” The researchers focused on epidermal keratinocytes, the main cells of the outer protective layer of the skin which is strongly impaired in the skin of elderly. EVs were purified from conditioned medium of primary keratinocytes isolated from infant or aged adult skin. A significant increase of the relative number of EVs released from aged keratinocytes was observed whereas their size distribution was not modified. By small RNA sequencing, the researchers described a specific microRNA (miRNA) signature of aged EVs with an increase abundance of miR-30a, a key regulator of barrier function in human epidermis. EVs from aged keratinocytes were found to be able to reduce the proliferation of young keratinocytes, to impact their organogenesis properties in a reconstructed epidermis model and to slow down the early steps of skin wound healing in mice, three features observed in aged epidermis. This work reveals that intercellular communication mediated by EVs is modulated during aging process in keratinocytes and might be involved in the functional defects observed in aged skin. “To conclude, we have shown here that aging modulates EVs abundance, function and microRNA content in human keratinocytes.” DOI - https://doi.org/10.18632/aging.205245 Corresponding author - Jérôme Lamartine - jerome.lamartine@univ-lyon1.fr Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205245 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, keratinocytes, microRNA, senescence, exosomes About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- November 28, 2023 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 21, entitled, “1,5-anhydro-D-fructose induces anti-aging effects on aging-associated brain diseases by increasing 5’-adenosine monophosphate-activated protein kinase activity via the peroxisome proliferator-activated receptor-γ co-activator-1α/brain-derived neurotrophic factor pathway.” 5’-Adenosine monophosphate-activated protein kinase (AMPK) is a metabolic sensor that serves as a cellular housekeeper; it also controls energy homeostasis and stress resistance. Thus, correct regulation of this factor can enhance health and survival. AMPK signaling may have a critical role in aging-associated brain diseases. Some in vitro studies have shown that 1,5-anhydro-D-fructose (1,5-AF) induces AMPK activation. In this new study, researchers Kiyoshi Kikuchi, Shotaro Otsuka, Seiya Takada, Kazuki Nakanishi, Kentaro Setoyama, Harutoshi Sakakima, Eiichiro Tanaka, and Ikuro Maruyama from Kagoshima University investigated the effects of 1,5-AF on the AMPK/PGC-1α/BDNF pathway in multiple animal models of human aging-associated brain diseases. “In the present study, we experimentally evaluated the effects of 1,5-AF on aging-associated brain diseases in vivo using an animal model of acute ischemic stroke (AIS), stroke-prone spontaneously hypertensive rats (SHRSPs), and the spontaneous senescence-accelerated mouse-prone 8 (SAMP8) model.” In the AIS model, intraperitoneal injection of 1,5-AF reduced cerebral infarct volume, neurological deficits, and mortality. In SHRSPs, oral administration of 1,5-AF reduced blood pressure and prolonged survival. In the SAMP8 model, oral administration of 1,5-AF alleviated aging-related decline in motor cognitive function. Although aging reduced the expression levels of peroxisome proliferator-activated receptor-γ co-activator-1α (PGC-1α) and brain-derived neurotrophic factor (BDNF), the researchers found that 1,5-AF activated AMPK, which led to upregulation of the PGC-1α/BDNF pathway. “Our results suggest that 1,5-AF can induce endogenous neurovascular protection, potentially preventing aging-associated brain diseases. Clinical studies are needed to determine whether 1,5-AF can prevent aging-associated brain diseases.” DOI - https://doi.org/10.18632/aging.205228 Corresponding authors - Kiyoshi Kikuchi - kikuchi_kiyoshi@kurume-u.ac.jp, and Ikuro Maruyama - maruyama-i@eva.hi-ho.ne.jp Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205228 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, AMP-activated protein kinases, brain-derived neurotrophic factor, peroxisome proliferator-activated receptors, blood pressure About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM