Aging-US

BUFFALO, NY- May 24, 2022 – Aging (Aging-US) is sponsoring the Systems Aging Gordon Research Conference, “Systemic Processes, Omics Approaches and Biomarkers in Aging,” from May 29 to June 3, 2022, at the Grand Summit Hotel at Sunday River in Newry, Maine, USA. This year, the Chair and Vice Chair of the conference are Aging Editorial Board members Vadim N. Gladyshev, Professor of Medicine at Harvard Medical School and Director of Redox Medicine at Brigham and Women’s Hospital, and Steve Horvath, Professor of Human Genetics and Biostatistics at the University of California, Los Angeles. Dr. Gladyshev is known for his characterization of the human selenoproteome. He was also elected as a member of the U. S. National Academy of Sciences in 2021. Dr. Horvath is a world-renowned researcher, geneticist and biostatistician. Recently, Aging devoted a research collection to Dr. Horvath’s profound contributions in epigenetics and DNA methylation research. Read Aging’s Special Collection on Steve Horvath Publications: https://www.aging-us.com/special-collections-archive/steve-horvath. Both Drs. Gladyshev and Horvath will be speaking and leading discussions at this meeting. In addition, a number of prestigious researchers from renowned institutions will be presenting at this conference. Presenters who are also members of Aging’s Editorial Board include Cynthia Kenyon, Manuel Serrano, Alex Zhavoronkov, and Vera Gorbunova. Over the course of the six-day Systems Aging Gordon Research Conference, presentations will cover many topics, including delaying aging, aging clocks, clinical biomarkers, advances in systemic rejuvenation, comparative and multi-omics approaches, applications of machine learning and artificial intelligence, the current understanding of the molecular basis of aging, and longevity interventions in model organisms. The organizers of the conference hope this meeting will facilitate deep discussions and the free exchange of ideas between not only established researchers but also junior scientists. “The 2022 Systems Aging GRC will set the stage for subsequent meetings and future development of this field, with the idea to ultimately help delay and reverse aging and age-related pathology.” (Source: 2022 Systems Aging GRC) About Aging-US: Launched in 2009, Aging (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 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. Follow Aging on social media: SoundCloud – https://soundcloud.com/Aging-Us Facebook – https://www.facebook.com/AgingUS/ Twitter – https://twitter.com/AgingJrnl Instagram – https://www.instagram.com/agingjrnl/ YouTube – https://www.youtube.com/agingus​ LinkedIn – https://www.linkedin.com/company/aging/ Pinterest – https://www.pinterest.com/AgingUS/ For media inquiries, please contact media@impactjournals.com.

In 2000 and 2011, Drs. Douglas Hanahan and Robert Weinberg authored two papers which stand as the original hallmarks of cancer. Since then, the hallmarks of cancer have been used as a critical framework to develop effective new cancer theranostics. In 2013, López-Otín et al. used the hallmarks of cancer in an effort to construct hallmarks of aging. However, in 2021, Drs. David Gems and João Pedro de Magalhães authored a paper critiquing the hallmarks of aging as a paradigm and urging researchers to move beyond the hallmarks to better understand the process of aging. On May 9, 2022, Dr. Mikhail Blagosklonny published an original review paper in Aging (Aging-US) Volume 14, Issue 9, entitled, “Hallmarks of cancer and hallmarks of aging.” Dr. Blagosklonny expands on Gems and de Magalhães’ sentiment and writes that “canonic hallmarks of aging are superficial imitations of the hallmarks of cancer.” He takes their work to the next level by offering his own original concept that rearranges the hallmarks of cancer and the hallmarks of aging based on the hierarchical principle and the hyperfunction theory of aging. “According to hyperfunction theory, aging is a continuation of developmental and reproductive programs that were not turned off upon their completion.” Full blog - https://aging-us.org/2022/05/an-original-review-on-the-hallmarks-of-cancer-and-aging/ DOI - https://doi.org/10.18632/aging.204082 Corresponding author - Mikhail V. Blagosklonny - Blagosklonny@oncotarget.com, Blagosklonny@rapalogs.com Press release - https://aging-us.com/news_room/hallmarks-of-cancer-and-hallmarks-of-aging-reviewed Keywords - aging, oncology, carcinogenesis, geroscience, mTOR, rapamycin, hyperfunction theory 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 http://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus​ LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com​​ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- May 18, 2022 – Dr. Mikhail Blagosklonny published his new review paper in Aging (Aging-US) Volume 14, Issue 9, entitled, “Hallmarks of cancer and hallmarks of aging.” In this review, Dr. Blagosklonny expands on Gems and de Magalhães’ notion that canonic hallmarks of aging are superficial imitations of the hallmarks of cancer. He takes their work a step further and proposes the hallmarks of cancer and aging based on a hierarchical principle and the hyperfunction theory. “Here I present the hallmarks of cancer, depicted as a circle by Hanahan and Weinberg [1], not as the circle but hierarchically, from molecular levels to the organism (Figure 1).” Next, Dr. Blagosklonny depicts the hallmarks of aging suggested by López-Otín et al. based on the hierarchical principle. “This representation renders hallmarks tangible but reveals three shortcomings (Figure 2).” The first shortcoming that Dr. Blagosklonny notes is the lack of hallmarks on the organismal level. The second is that the relationship between hallmarks on different levels is unclear. The third is that the inclusion of genetic instability as a hallmark is based on the theory that aging is caused by the accumulation of molecular damage. “The molecular damage theory was refuted by key experiments, as discussed in detail [44–51].” Dr. Blagosklonny then uses the hyperfunction theory to arrange the hierarchical hallmarks of aging. “Let us depict hallmarks of aging, according to the hyperfunction theory of aging (Figure 3).” Dr. Blagosklonny continues by discussing the key to understanding aging and aging as a selective force for cancer. He concludes this review by discussing the common hallmarks of cancer, aging and cell senescence. “In organismal aging, cancer and cellular senescence, the same key signaling pathways, such as mTOR, are involved. This is why the same drugs, such as rapamycin, can suppress all of them.” DOI: https://doi.org/10.18632/aging.204082 Correspondence to: Mikhail V. Blagosklonny Email: Blagosklonny@oncotarget.com, Blagosklonny@rapalogs.com Keywords: oncology, carcinogenesis, geroscience, mTOR, rapamycin, hyperfunction theory Follow Dr. Blagosklonny on Twitter: https://twitter.com/Blagosklonny 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. Follow Aging on social media: SoundCloud – https://soundcloud.com/Aging-Us Facebook – https://www.facebook.com/AgingUS/ Twitter – https://twitter.com/AgingJrnl Instagram – https://www.instagram.com/agingjrnl/ YouTube – https://www.youtube.com/agingus​ LinkedIn – https://www.linkedin.com/company/aging/ Pinterest – https://www.pinterest.com/AgingUS/ For media inquiries, please contact media@impactjournals.com.

A new research paper was published on the cover of Aging (Aging-US) Volume 14, Issue 9, entitled, “Single-cell transcriptomics reveals age-resistant maintenance of cell identities, stem cell compartments and differentiation trajectories in long-lived naked mole-rats skin.” Researchers who authored this research paper are affiliated with the Université Paris Cité, Sorbonne Université, Fondation pour la Recherche en Physiologie, Queen Mary University of London, Hôpital Tenon, Université de Namur ASBL, Ecole Nationale Vétérinaire d’Alfort, and Hôpital Cochin. “In the present study, we performed extensive in situ analysis and single-cell RNA-sequencing comparing young and older animals.” Skin acts as an essential barrier and protects organisms from external threats, preventing fluid loss, stabilizing body temperature and relaying sensory information to the brain. Maintaining skin homeostasis is essential, as alterations in skin functions can cause various deleterious conditions ranging from fluid loss to more severe diseases, such as infections or UV-induced cancers. Naked mole-rats (NMR) are subterranean rodents characterized by an unusual longevity coupled with an unexplained resistance to aging. At variance with other species, naked mole-rats exhibited a striking stability of skin compartments and cell types, which remained stable over time without aging-associated changes. “Thus, we hypothesize that the maintenance of cellular compartments in the older NMR, especially the stem cell pool through high Igfbp3 expression, coupled with an increase skin immunity, could explain their skin slower rate of aging.” The researchers used single-cell RNA-sequencing (scRNA-seq) to obtain an unbiased molecular RNA profile of the naked mole-rats’ epidermal cell populations. They found that epidermal gene expression did not change with aging. Three classical cellular states defined a unique keratinocyte differentiation trajectory that were not altered after pseudo-temporal reconstruction. NMR skin healing closure was similar in young and older animals and, remarkably, the number of stem cells was constant throughout aging. The researchers found that NMR epidermal cells displayed two main populations, immune cells (one cluster) and keratinocytes, subdivided into 10 clusters. “Performing a deeper analysis within each cluster individually, we found 2 genes overexpressed in basal stem cells of older animals and 5 genes overexpressed in immune cells of older animals.” “Altogether, these results indicate that NMR skin is characterized by peculiar genetic and cellular features, different from those previously demonstrated for mice and humans. The remarkable stability of the aging NMR skin transcriptome likely reflects unaltered homeostasis and resilience.” DOI: https://doi.org/10.18632/aging.204054 Correspondence to: Romain H. Fontaine Email: romain.fontaine@inserm.fr Keywords: naked mole-rat, skin stem cells, wound healing, aging 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. Follow Aging on social media: SoundCloud – https://soundcloud.com/Aging-Us Facebook – https://www.facebook.com/AgingUS/ Twitter – https://twitter.com/AgingJrnl Instagram – https://www.instagram.com/agingjrnl/ YouTube – https://www.youtube.com/agingus​ LinkedIn – https://www.linkedin.com/company/aging/ Pinterest – https://www.pinterest.com/AgingUS/ For media inquiries, please contact media@impactjournals.com.

Listen to a blog summary of Dr. Blagosklonny's latest research perspective published in Oncoscience, entitled, “Altos Labs and the quest for immortality: but can we live longer right now?” ___________________________ After the January 2022 launch of Altos Labs, a new anti-aging biotechnology company, Mikhail (Misha) Blagosklonny, M.D., Ph.D., joined this exciting public conversation with a recommendation. Dr. Blagosklonny is a prominent scientist in the fields of cancer and aging research. He is well-known for his experimental research articles and theoretical papers on the hyperfunction theory of aging and the pursuit of longevity with rapamycin. On April 22, 2022, his latest research perspective was published in Oncoscience, and entitled, “Altos Labs and the quest for immortality: but can we live longer right now?” Full blog - https://aging-us.org/2022/05/dr-blagosklonnys-rapamycin-based-recommendation-for-altos-labs/ DOI - https://doi.org/10.18632/oncoscience.552 Corresponding author - Mikhail V. Blagosklonny - Blagosklonny@oncotarget.com, Blagosklonny@rapalogs.com Keywords - aging, longevity, lifespan, geroscience, rapalogs, gerostatics 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 http://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus​ LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com​​ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- May 11, 2022 – A new research perspective was published in Oncoscience journal by Mikhail Blagosklonny, M.D., Ph.D., entitled, “Altos Labs and the quest for immortality: but can we live longer right now?” “Here I discuss how combining rapamycin with other modalities may let us live long enough to benefit from future discoveries in cellular reprogramming and what needs to be done at Altos Labs to make this happen.” Altos Labs—a new anti-aging biotechnology company funded by multiple billionaire investors, including Jeff Bezos and Yuri Milner—has reported a focus on reprogramming cells in order to reverse the trajectory of diseases, and thus, reverse aging. In his research perspective, Dr. Blagosklonny writes that potential life-extension with rapamycin may allow us to win time while awaiting future discoveries that will reverse aging. “Rapamycin treatment is rapidly becoming a mainstream anti-aging intervention.” However, Dr. Blagosklonny also writes that rapamycin alone is unlikely to extend lifespan sufficiently to benefit from Altos Labs’ future discoveries in our lifetime. “If Altos Labs would allocate a small percentage of its funding to develop rapamycin based drug combinations, then additional decades of life extension may be available 3–5 years from now.” “The number of potential combinations with rapamycin is enormous.” Read Dr. Blagosklonny’s research perspective: https://www.oncoscience.us/article/552/text/ Correspondence to: Mikhail V. Blagosklonny Email: Blagosklonny@oncotarget.com, Blagosklonny@rapalogs.com Keywords: aging, longevity, lifespan, geroscience, rapalogs, gerostatics Follow Dr. Blagosklonny on Twitter: https://twitter.com/Blagosklonny For media inquiries, please contact media@impactjournals.com. Oncoscience Journal Office 6666 East Quaker Str., Suite 1D Orchard Park, NY 14127 Phone: 1-800-922-0957, option 4 ###

Listen to a blog summary of a research paper selected as the cover for Volume 14, Issue 8, entitled, "Wild type and gain of function mutant TP53 can regulate the sensitivity of pancreatic cancer cells to chemotherapeutic drugs, EGFR/Ras/Raf/MEK, and PI3K/mTORC1/GSK-3 pathway inhibitors, nutraceuticals and alter metabolic properties." __________________________ Patients over the age of 50 years old who have been diagnosed with pancreatic cancer have a poorer rate of survival compared to younger patients. This means that pancreatic cancer is a disease associated with aging. The most common type of pancreatic cancer is pancreatic ductal adenocarcinoma (PDAC) and it is frequently diagnosed in its later stages. PDAC is often refractive to chemotherapies and develops resistance to inhibitors and other drugs. Therefore, there is a critical need for researchers to discover novel strategies to overcome drug resistance in PDAC cells. One potential strategy is to focus on a key gene known for its involvement in many cell processes, including drug resistance and metabolism: TP53. The TP53 gene is often mutated or deleted in cancer cells, which can lead to drug resistance and cancer metastasis. In PDACS, this tumor suppressor gene has been shown to be mutated in 50–75% of patients. “Many genes have been implicated in PDAC including KRAS, TP53, CDKN2A, SMAD4 and PDGFβR [3, 8, 9, 18–22].” In a new study, researchers—from Brody School of Medicine at East Carolina University, Università di Bologna, University of Parma, and University of Wroclaw—further elucidated TP53’s role in drug resistance in PDAC cells. On April 27, 2022, their research paper was published in Aging (Aging-US) on the cover of Volume 14, Issue 8, and entitled, “Wild type and gain of function mutant TP53 can regulate the sensitivity of pancreatic cancer cells to chemotherapeutic drugs, EGFR/Ras/Raf/MEK, and PI3K/mTORC1/GSK-3 pathway inhibitors, nutraceuticals and alter metabolic properties.” Full blog - https://aging-us.org/2022/05/tp53-restoration-sensitizes-pancreatic-cancer-to-multiple-drugs/ DOI - https://doi.org/10.18632/aging.204038 Corresponding author - James A. McCubrey - mccubreyj@ecu.edu Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204038 Keywords - aging, TP53, targeted therapy, PDAC, metabolic properties, chemotherapeutic drugs 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 http://www.Aging-US.com​​ or connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus​ LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com​​ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

Listen to a blog summary of a trending research paper published by Aging (Aging-US) in Volume 14, Issue 7, entitled, “The tobacco phosphatidylethanolamine-binding protein NtFT4 increases the lifespan of Drosophila melanogaster by interacting with the proteostasis network.” ___________________________ Full blog - https://aging-us.org/2022/04/trending-with-impact-tobacco-pebp-increases-lifespan-in-fruit-flies/ DOI - https://doi.org/10.18632/aging.204005 Corresponding author - Philip Känel - philip.kaenel@ime.fraunhofer.de Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204005 Keywords - aging, proteostasis, heat shock proteins, chaperone, locomotor activity 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 http://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus​ LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com​​ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

Listen to a blog summary of a trending research paper selected as the cover for Volume 14, Issue 7 of Aging (Aging-US), entitled, "Downregulation of IGFBP5 contributes to replicative senescence via ERK2 activation in mouse embryonic fibroblasts." ___________________________________ In 1961, Leonard Hayflick and Paul Moorhead proposed a theory later named the Hayflick Limit. They discovered that a normal human cell can divide between 50 and 70 times before it can no longer proliferate and eventually dies. Researchers have since continued to explore this phenomenon and, today, this aging process is known as cellular (replicative) senescence. “There are currently several experimental models of cellular senescence. Hayflick and Moorhead observed that primary human fibroblasts in culture exhibit a limited proliferative capacity [6]. This growth arrest during passages is called replicative senescence.” This permanent cessation of the cell cycle is universally found in biology due to known and unknown causes, including the shortening of telomeres. While telomere shortening plays an important role, it is not the only event responsible for inducing cellular senescence. Thus, researchers have spent decades under the microscope experimenting with cellular models of replicative senescence. In a new study released on April 4, 2022, researchers from Sapporo Medical University in Sapporo, Japan, investigated mechanisms of replicative senescence in vitro. Their research paper was published on the cover of Aging (Aging-US) Volume 14, Issue 7, and entitled, “Downregulation of IGFBP5 contributes to replicative senescence via ERK2 activation in mouse embryonic fibroblasts.” Full blog - https://aging-us.org/2022/04/trending-with-impact-underlying-mechanisms-of-replicative-senescence/ DOI - https://doi.org/10.18632/aging.203999 Corresponding author - Atsushi Kuno - kuno@sapmed.ac.jp Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.20399 Keywords - aging, IGFBP5, replicative senescence, mouse embryonic fibroblasts, ERK2, ERK1 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 http://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus​ LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com​​ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

Listen to a blog summary of this priority research paper published in Volume 13, Issue 11, entitled, "GRSF1 deficiency in skeletal muscle reduces endurance in aged mice." ________________________________ Skeletal muscle is responsible for regulating physical movement and comprises between 30 and 40% of the human body’s mass. The loss of skeletal muscle has major impacts on overall health and quality of life—leading to frailty and a decreased ability to perform activities of daily living. The most common cause of muscle loss is aging, and a prevalent pattern of aging-associated muscular decline is known as sarcopenia. “With advancing age, the progressive loss of skeletal muscle mass and function, known as sarcopenia, leads to reduced muscle strength and diminishes individual mobility, quality of life, and lifespan [12].” In a research paper published in Aging (Aging-US) Volume 13, Issue 11, researchers from National Institutes of Health’s National Institute on Aging and Chungnam National University investigated a protein that may play a role in aging-related muscle loss. Their paper was published on June 2, 2021, and entitled, “GRSF1 deficiency in skeletal muscle reduces endurance in aged mice.” Full blog - https://aging-us.org/2022/04/protein-linked-to-aging-related-muscle-loss/ DOI - https://doi.org/10.18632/aging.203151 Corresponding authors - Chang-Yi Cui - cuic@grc.nia.nih.gov, and Myriam Gorospe - myriam-gorospe@nih.gov Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.203151 Keywords - aging, skeletal muscle aging, GRSF1, RNA-binding protein, mouse aging 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 http://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus​ LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com​​ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM