

Aging-US
Aging (Aging-US) Podcast
Aging-US is dedicated to advancing our understanding of the biological mechanisms that drive aging and the development of age-related diseases. Our mission is to serve as a platform for high-quality research that uncovers the cellular, molecular, and systemic processes underlying aging, and translates these insights into strategies to extend healthspan and delay the onset of chronic disease.
Read about the Aging (Aging-US) Scientific Integrity Process: https://aging-us.com/scientific-integrity
Read about the Aging (Aging-US) Scientific Integrity Process: https://aging-us.com/scientific-integrity
Episodes
Mentioned books

Mar 12, 2024 • 3min
Association of Prenatal Vitamins and Metals With Epigenetic Aging at Birth and in Childhood
BUFFALO, NY- March 12, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 4, entitled, “Associations of prenatal one-carbon metabolism nutrients and metals with epigenetic aging biomarkers at birth and in childhood in a US cohort.”
Epigenetic gestational age acceleration (EGAA) at birth and epigenetic age acceleration (EAA) in childhood may be biomarkers of the intrauterine environment. In this new study, researchers Anne K. Bozack, Sheryl L. Rifas-Shiman, Andrea A. Baccarelli, Robert O. Wright, Diane R. Gold, Emily Oken, Marie-France Hivert, and Andres Cardenas from Stanford University School of Medicine, Harvard Medical School, Harvard T.H. Chan School of Public Health, Columbia University, and Icahn School of Medicine at Mount Sinai investigated the extent to which first-trimester folate, B12, 5 essential and 7 non-essential metals in maternal circulation are associated with EGAA and EAA in early life.
“[...] we hypothesized that OCM [one-carbon metabolism] nutrients and essential metals would be positively associated with EGAA and non-essential metals would be negatively associated with EGAA. We also investigated nonlinear associations and associations with mixtures of micronutrients and metals.”
Bohlin EGAA and Horvath pan-tissue and skin and blood EAA were calculated using DNA methylation measured in cord blood (N=351) and mid-childhood blood (N=326; median age = 7.7 years) in the Project Viva pre-birth cohort. A one standard deviation increase in individual essential metals (copper, manganese, and zinc) was associated with 0.94-1.2 weeks lower Horvath EAA at birth, and patterns of exposures identified by exploratory factor analysis suggested that a common source of essential metals was associated with Horvath EAA. The researchers also observed evidence of nonlinear associations of zinc with Bohlin EGAA, magnesium and lead with Horvath EAA, and cesium with skin and blood EAA at birth. Overall, associations at birth did not persist in mid-childhood; however, arsenic was associated with greater EAA at birth and in childhood.
“Prenatal metals, including essential metals and arsenic, are associated with epigenetic aging in early life, which might be associated with future health.”
DOI - https://doi.org/10.18632/aging.205602
Corresponding author - Andres Cardenas - andres.cardenas@stanford.edu
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Keywords - aging, epigenetic age acceleration, metals, folate, B12, prenatal exposures
About Aging-US
Aging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.
Please visit our website at https://www.Aging-US.com and connect with us:
Facebook - https://www.facebook.com/AgingUS/
X - https://twitter.com/AgingJrnl
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YouTube - https://www.youtube.com/@AgingJournal
LinkedIn - https://www.linkedin.com/company/aging/
Pinterest - https://www.pinterest.com/AgingUS/
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Mar 11, 2024 • 2min
Aging at AACR Annual Meeting 2024
BUFFALO, NY- March 11, 2024 – Impact Journals #publishes scholarly #journals in the #biomedical sciences with a focus on all areas of cancer and aging research. Aging is one of the most prominent journals published by Impact Journals.
Impact Journals will be participating as an exhibitor at the American Association for Cancer Research (AACR) Annual Meeting 2024 from April 5-10 at the San Diego Convention Center in San Diego, California. This year, the AACR meeting theme is “Inspiring Science • Fueling Progress • Revolutionizing Care.”
Visit booth number 4159 at the AACR Annual Meeting 2024 to connect with members of the Aging team.
Aging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.
Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed Central, Web of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).
Please visit our website at https://www.Aging-US.com and connect with us:
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Mar 11, 2024 • 9min
Behind the Study: Analyzing Psoriasis Communication Patterns for Treatment Optimization
Dr. Jiajian Wang from Sun Yat-Sen University, The Chinese University of Hong Kong, the Chinese Academy of Sciences, and the Shenzhen Key Laboratory of Metabolic Health, describes a #research paper he co-authored and #published in Aging’s Volume 16, Issue 3, entitled, “Generating detailed intercellular communication patterns in psoriasis at the single-cell level using social networking, pattern recognition, and manifold learning methods to optimize treatment strategies.”
Here is an audio version of a written Q&A that was submitted by Dr. Jiajian Wang on this research.
Full Q&A - https://aging-us.net/2024/03/11/behind-the-study-analyzing-psoriasis-communication-patterns-for-treatment-optimization/
Paper DOI - https://doi.org/10.18632/aging.205478
Corresponding Authors - Jiajian Wang - jiajianwang2019@gmail.com, and Bo Wu - bowu2004@hotmail.com
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Keywords - communication patterns, single cell transcriptome, cell type-specific regulons (CTSRs), proteomic sequencing, social networking
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:
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/
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Mar 7, 2024 • 8min
Overcoming Missing Data in the Swedish National Study on Aging
Missing data in aging studies, especially in the assessment of gait speed (the time it takes individuals to cover a set distance), presents a significant challenge. The elderly are more prone to health and functional issues, which often interfere with data collection efforts. Given that gait speed is a key indicator of functional status and overall health in older individuals, ensuring its availability and accurate measurement is essential for the integrity of aging research.
In a new study, researchers Robert Thiesmeier, Ahmad Abbadi, Debora Rizzuto, Amaia Calderón-Larrañaga, Scott M. Hofer, and Nicola Orsini from Karolinska Institutet, Stockholm University, Stockholm Gerontology Research Center, and Oregon Health and Science University address the systematic challenge of missing gait speed data in aging research and explore the application of multiple imputation (MI), a statistical technique that has emerged as a constructive approach to handle such gaps in data. The team critically examined the implementation strategies, methodologies, and the impact that these missing variables could have on the outcomes of aging studies, thereby offering a framework to manage and interpret incomplete datasets in aging research. On February 14, 2024, their research paper was published in Aging’s Volume 16, Issue 4, entitled, “Multiple imputation of systematically missing data on gait speed in the Swedish National Study on Aging and Care.”
“[...] this study aims to investigate and assess the performance of different MI strategies specifically targeting the systematically missing discrete variable of gait speed in the SNAC [Swedish National Study on Aging and Care] IPDMA [individual participant data meta-analyses] with only four large cohort studies.”
Full blog - https://aging-us.org/2024/03/overcoming-missing-data-in-the-swedish-national-study-on-aging/
Paper DOI - https://doi.org/10.18632/aging.205552
Corresponding authors - Robert Thiesmeier - robert.thiesmeier@ki.se
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Keywords - aging, simulation, systematically missing values, individual participant data, meta-analysis, gait speed
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:
Facebook - https://www.facebook.com/AgingUS/
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LinkedIn - https://www.linkedin.com/company/aging/
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Mar 6, 2024 • 4min
A Longitudinal Study on Dasatinib, Quercetin, and Fisetin Senolytic Interventions
BUFFALO, NY- March 6, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 4, entitled, “Exploring the effects of Dasatinib, Quercetin, and Fisetin on DNA methylation clocks: a longitudinal study on senolytic interventions.”
Senolytics, small molecules targeting cellular senescence, have emerged as potential therapeutics to enhance health span. However, their impact on epigenetic age remains unstudied. In this new study, researchers Edwin Lee, Natàlia Carreras-Gallo, Leilani Lopez, Logan Turner, Aaron Lin, Tavis L. Mendez, Hannah Went, Alan Tomusiak, Eric Verdin, Michael Corley, Lishomwa Ndhlovu, Ryan Smith, and Varun B. Dwaraka from the Institute For Hormonal Balance, TruDiagnostic, Buck Institute for Research on Aging, and Cornell University aimed to assess the effects of senolytic treatments on DNA methylation (DNAm), epigenetic age, and immune cell subsets.
“[...] this study aims to comprehensively assess the impact of senolytic drugs on epigenetic aging through two longitudinal studies to address our research objective. The initial investigation focuses on a combination treatment of Dasatinib and Quercetin, while the subsequent phase incorporates Fisetin into the treatment regimen.”
In a Phase I pilot study, 19 participants received Dasatinib and Quercetin (DQ) for 6 months, with DNAm measured at baseline, 3 months, and 6 months. Significant increases in epigenetic age acceleration were observed in first-generation epigenetic clocks and mitotic clocks at 3 and 6 months, along with a notable decrease in telomere length. However, no significant differences were observed in second and third-generation clocks.
Building upon these findings, a subsequent investigation evaluated the combination of DQ with Fisetin (DQF), a well-known antioxidant and antiaging senolytic molecule. After one year, 19 participants (including 10 from the initial study) received DQF for 6 months, with DNAm assessed at baseline and 6 months. Remarkably, the addition of Fisetin to the treatment resulted in non-significant increases in epigenetic age acceleration, suggesting a potential mitigating effect of Fisetin on the impact of DQ on epigenetic aging.
“Furthermore, our analyses unveiled notable differences in immune cell proportions between the DQ and DQF treatment groups, providing a biological basis for the divergent patterns observed in the evolution of epigenetic clocks. These findings warrant further research to validate and comprehensively understand the implications of these combined interventions.”
DOI - https://doi.org/10.18632/aging.205581
Corresponding authors - Varun B. Dwaraka - varun@trudiagnostic.com
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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:
Facebook - https://www.facebook.com/AgingUS/
X - https://twitter.com/AgingJrnl
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YouTube - https://www.youtube.com/@AgingJournal
LinkedIn - https://www.linkedin.com/company/aging/
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Mar 5, 2024 • 3min
A Call for Standardization of Controls in Lifespan Studies
BUFFALO, NY- March 5, 2024 – A new #research perspective was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 4, entitled, “On standardization of controls in lifespan studies.”
In this new paper, researchers Olga Spiridonova, Dmitrii Kriukov, Nikolai Nemirovich-Danchenko, and Leonid Peshkin from Harvard Medical School's Department of Systems Biology discuss the burgeoning field of the search for interventions to slow down, and even reverse, aging. Currently available literature cites hundreds of supposedly beneficial pharmacological and genetic interventions in model organisms: mice, rats, flies, and worms, where research into physiology is routinely accompanied by lifespan data. However, when experimental animals from one article live as long as controls from another article, comparing the results of interventions across studies can yield misleading outcomes.
“Theoretically, all lifespan data are ripe for re-analysis: we could contrast the molecular targets and pathways across studies and help focus the further search for interventions.”
Alas, the results of most longevity studies are difficult to compare. This is in part because there are no clear, universally accepted standards for conducting such experiments or even for reporting such data. The situation is worsened by the fact that the authors often do not describe experimental conditions completely. As a result, works on longevity make up a set of precedents, each of which might be interesting in its own right, yet incoherent and incomparable at least for the reason that in a general context, it may indicate, for example, not prolonging the life of an average organism, but compensating for any genetic abnormalities of a particular sample or inappropriate living conditions.
“Here we point out specific issues and propose solutions for quality control by checking both inter- and intra-study consistency of lifespan data.”
DOI - https://doi.org/10.18632/aging.205604
Corresponding author - Leonid Peshkin - pesha@hms.harvard.edu
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Keywords - aging, animal disease models, survival modeling, data standardization
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:
Facebook - https://www.facebook.com/AgingUS/
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LinkedIn - https://www.linkedin.com/company/aging/
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Feb 29, 2024 • 4min
Mapping the Core Senescence Phenotype of Human Colon Fibroblasts
BUFFALO, NY- February 29, 2024 – A new #research paper was #published on the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 4, entitled, “Mapping the core senescence phenotype of primary human colon fibroblasts.”
Advanced age is the largest risk factor for many diseases and several types of cancer, including colorectal cancer (CRC). Senescent cells are known to accumulate with age in various tissues, where they can modulate the surrounding tissue microenvironment through their senescence associated secretory phenotype (SASP). Recently, researchers showed that there is an increased number of senescent cells in the colons of CRC patients and demonstrated that senescent fibroblasts and their SASP create microniches in the colon that are conducive to CRC onset and progression. However, the composition of the SASP is heterogenous and cell-specific, and the precise senescence profile of colon fibroblasts has not been well-defined.
In this new study, to generate a SASP atlas of human colon fibroblasts, researchers Namita Ganesh Hattangady, Kelly Carter, Brett Maroni-Rana, Ting Wang, Jessica Lee Ayers, Ming Yu, and William M. Grady from Fred Hutchinson Cancer Center and the University of Washington School of Medicine induced senescence in primary human colon fibroblasts using various in vitro methods and assessed the resulting transcriptome.
“[...] we utilized various relevant stressors to induce senescence in primary cultures of colon fibroblasts and perform RNA sequencing (RNASeq) to define an atlas of stressor-specific senescent profiles and a core senescent profile that is commonly regulated by all senescence inducers.”
Using RNA Sequencing and further validation by quantitative RT-PCR and Luminex assays, the team define and validate a ‘core senescent profile’ that might play a significant role in shaping the colon microenvironment. They also performed KEGG analysis and GO analyses to identify key pathways and biological processes that are differentially regulated in colon fibroblast senescence. These studies provide insights into potential driver proteins involved in senescence-associated diseases, like CRC, which may lead to therapies to improve overall health in the elderly and to prevent CRC.
“Further studies will be needed to address the limitations of our study and to translate our understanding of the SASP and disease into clinical care.”
DOI - https://doi.org/10.18632/aging.205577
Corresponding authors - William M. Grady - wgrady@fredhutch.org, and Ming Yu - myu@fredhutch.org
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Keywords - aging, senescence, senescence associated secretory phenotype, SASP, colorectal cancer, cancer
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:
Facebook - https://www.facebook.com/AgingUS/
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YouTube - https://www.youtube.com/@AgingJournal
LinkedIn - https://www.linkedin.com/company/aging/
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Feb 28, 2024 • 6min
Prognostic Model Development and Molecular Subtypes Identification in Bladder Urothelial Cancer
BUFFALO, NY- February 28, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 3, entitled, “Prognostic model development and molecular subtypes identification in bladder urothelial cancer by oxidative stress signatures.”
Mounting studies indicate that oxidative stress (OS) significantly contributes to tumor progression. In this new study, researchers Ying Dong, Xiaoqing Wu, Chaojie Xu, Yasir Hameed, Mostafa A. Abdel-Maksoud, Taghreed N. Almanaa, Mohamed H. Kotob, Wahidah H. Al-Qahtani, Ayman M. Mahmoud, William C. Cho, and Chen Li from Shenzhen Second People’s Hospital, China Academy of Chinese Medical Sciences, Peking University, The Islamia University of Bahawalpur, King Saud University, University of Vienna, Manchester Metropolitan University, Queen Elizabeth Hospital, and Free University of Berlin focused on bladder urothelial cancer (BLCA), an escalating malignancy worldwide that is growing rapidly.
“Our objective was to verify the predictive precision of genes associated with overall survival (OS) by constructing a model that forecasts outcomes for bladder cancer and evaluates the prognostic importance of these genetic markers.”
Full press release - https://www.aging-us.com/news-room/Prognostic-Model-Development-and-Molecular-Subtypes-Identification-in-Bladder-Urothelial-Cancer
DOI - https://doi.org/10.18632/aging.205499
Corresponding authors - Yasir Hameed - Yasirhameed2011@gmail.com, William C. Cho - chocs@ha.org.hk, and Chen Li - chen.li@fu-berlin.de
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Keywords - aging, oxidative stress, bladder urothelial cancer, tumor microenvironment, immunotherapy
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:
Facebook - https://www.facebook.com/AgingUS/
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Feb 27, 2024 • 3min
The Anti-aging Effect of Vitamin D and its Receptor in Drosophila Midgut
BUFFALO, NY- February 27, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 3, entitled, “The anti-aging effect of vitamin D and vitamin D receptor in Drosophila midgut.”
Adult stem cells are pivotal for maintaining tissue homeostasis, and their functional decline is linked to aging and its associated diseases, influenced by the niche cells’ environment. Age- and cancer-related reduction of vitamin D and its receptor levels are well documented in human clinical studies. However, the mechanisms through which the vitamin D/vitamin D receptor (VitD/VDR) pathway contributes to anti-aging and extends life expectancy are not well understood. In this new study, researchers Joung-Sun Park, Hyun-Jin Na and Yung-Jin Kim from Pusan National University and Korea Food Research Institute aimed to determine the protective role of the vitamin D/vitamin D receptor pathway in differentiated enterocytes (ECs) during intestinal stem cell (ISC) aging.
“This study aimed to determine the protective role of VitD/VDR in differentiated ECs during ISC aging using the adult Drosophila intestine model.”
By utilizing a well-established Drosophila midgut model for stem cell aging biology, the researchers revealed that vitamin D receptor knockdown in ECs induced ISC proliferation, EC death, ISC aging, and enteroendocrine cell differentiation. Additionally, age- and oxidative stress-induced increases in ISC proliferation and centrosome amplification were reduced by vitamin D treatment. In conclusion, this study provides direct evidence of the anti-aging role of the VitD/VDR pathway, involving protecting ECs during aging, and provides valuable insights for exploring the molecular mechanisms underlying enhanced healthy aging in Drosophila.
“Our findings suggest a direct evidence of the anti-aging role of the vitamin D/vitamin D receptor pathway and provides insights into the molecular mechanisms underlying healthy aging in Drosophila.”
DOI - https://doi.org/10.18632/aging.205518
Corresponding author - Joung-Sun Park - dreamjs78@pusan.ac.kr
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Keywords - aging, Drosophila, vitamin D, vitamin D receptor, anti-aging, intestinal stem cell
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:
Facebook - https://www.facebook.com/AgingUS/
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Feb 21, 2024 • 3min
Disruption of mtUPR Results in Telomere Shortening in Mouse Oocytes and Somatic Cells
BUFFALO, NY- February 21, 2024 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 3, entitled, “Disruption of mitochondrial unfolded protein response results in telomere shortening in mouse oocytes and somatic cells.”
Caseinolytic peptidase P (CLPP) plays a central role in mitochondrial unfolded protein response (mtUPR) by promoting the breakdown of misfolded proteins and setting in motion a cascade of reactions to re-establish protein homeostasis. Global germline deletion of Clpp in mice results in female infertility and accelerated follicular depletion. Telomeres are tandem repeats of 5’-TTAGGG-3’ sequences found at the ends of the chromosomes. Telomeres are essential for maintaining chromosome stability during somatic cell division and their shortening is associated with cellular senescence and aging.
In this new study, researchers Mauro Cozzolino, Yagmur Ergun, Emma Ristori, Akanksha Garg, Gizem Imamoglu, and Emre Seli from Yale School of Medicine, IVIRMA Global Research Alliance and Imperial College London asked whether the infertility and ovarian aging phenotype caused by global germline deletion of Clpp is associated with somatic aging, and tested telomere length in tissues of young and aging mice.
“In this study, we asked whether the infertility and ovarian aging phenotype caused by global germline deletion of Clpp is associated with somatic aging, and tested telomere length in young and aging mice gametes, gonads and somatic tissues.”
The team found that impaired mtUPR caused by the lack of CLPP is associated with accelerated telomere shortening in both oocytes and somatic cells of aging mice. In addition, expression of several genes that maintain telomere integrity was decreased, and double-strand DNA breaks were increased in telomeric regions. Their results highlight how impaired mtUPR can affect telomere integrity and demonstrate a link between loss of mitochondrial protein hemostasis, infertility, and somatic aging.
“Our findings demonstrate how loss of mitochondrial protein homeostasis may accelerate telomere shortening in oocytes and somatic cells, and provide a link between reproductive and somatic aging.”
DOI - https://doi.org/10.18632/aging.205543
Corresponding author - Emre Seli - emre.seli@yale.edu
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Keywords - aging, telomere length, Clpp, mitochondrial dysfunction, unfolded protein response
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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.
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