A twice-monthly, traditional, peer-reviewed, journal with open-access, covering all areas of research on aging, including age-related diseases, such as cancer.

Aging's (Aging-US) 2020 Impact Factor by Web of Science (Clarivate Analytics) is 5.682. This number has increased from last year’s 4.831. Without self-citation, Aging’s (Aging-US) 2020 Impact Factor is 5.279.

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 (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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Aging (Aging-US)

Aging-US published this trending review in Volume 14, Issue 9, entitled, "Hallmarks of cancer and hallmarks of aging" by Dr. Mikhail V. Blagosklonny from Roswell Park Comprehensive Cancer Center, Buffalo, NY. 

DOI - https://doi.org/10.18632/aging.204082

Corresponding author - Mikhail V. Blagosklonny - Blagosklonny@oncotarget.com, Blagosklonny@rapalogs.com

Abstract

A thought-provoking article by Gems and de Magalhães suggests that canonic hallmarks of aging are superficial imitations of hallmarks of cancer. I took their work a step further and proposed hallmarks of aging based on a hierarchical principle and the hyperfunction theory.

To do this, I first reexamine the hallmarks of cancer proposed by Hanahan and Weinberg in 2000. Although six hallmarks of cancer are genuine, they are not hierarchically arranged, i.e., molecular, intra-cellular, cellular, tissue, organismal and extra-organismal. (For example, invasion and angiogenesis are manifestations of molecular alterations on the tissue level; metastasis on the organismal level, whereas cell immortality is observed outside the host).

The same hierarchical approach is applicable to aging. Unlike cancer, however, aging is not a molecular disease. The lowest level of its origin is normal intracellular signaling pathways such as mTOR that drive developmental growth and, later in life, become hyperfunctional, causing age-related diseases, whose sum is aging. The key hallmark of organismal aging, from worms to humans, are age-related diseases. In addition, hallmarks of aging can be arranged as a timeline, wherein initial hyperfunction is followed by dysfunction, organ damage and functional decline.

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:

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Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com​​

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Paper Spotlight: Hallmarks of Cancer and Hallmarks of Aging

Aging (Aging-US) published this trending research perspective in Volume 14, Issue 7, entitled, “Heterochronic parabiosis: a valuable tool to investigate cellular senescence and other hallmarks of aging” by researchers from the Institute on the Biology of Aging and Metabolism, University of Minnesota, Minneapolis, MN; Department of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota, Minneapolis, MN; Department of Molecular Pharmacology and Medicine, Albert Einstein College of Medicine, Bronx, NY; Institute for Aging Research, Albert Einstein College of Medicine, Bronx, NY.

DOI - https://doi.org/10.18632/aging.204015

Corresponding authors - Matthew J. Yousefzadeh - myousefz@umn.edu, and Derek M. Huffman - derek.huffman@einsteinmed.org

Abstract

Parabiosis is a well-established method to facilitate a shared blood supply between two conjoined animals. In particular, the pairing of mice of dissimilar ages, termed heterochronic parabiosis, has been used extensively for differentiating cell autonomous and non-autonomous mechanisms of aging. Analysis of heterochronic parabionts also has helped to identify individual circulating factors that may act as either pro- or anti-geronics. Heterochronic parabiosis also has proven to be a valuable experimental system to evaluate the effects of specific hallmarks of aging on the process of aging. For example, heterochronic parabiosis was used recently to examine whether cellular senescence was driven via cell autonomous and/or non-autonomous mechanisms. As anticipated, markers of cellular senescence were elevated in old isochronically-paired mice relative to young controls. However, compared to old isochronically paired mice, the senescent cell burden was reduced in multiple tissues of old parabionts joined with young mice. This suggests that the rejuvenation of cells and tissues in old mice by exposure to young blood could be mediated, in part, through suppression or immune clearance of senescent cells. Conversely, young heterochronic parabionts showed increased markers of cellular senescence, demonstrating that exposure to an old circulation is able to drive senescence through a cell non-autonomous mechanism(s), likely contributing to accelerated aging in the young mice. Thus, heterochronic parabiosis is still an important methodology that should continue to be leveraged for evaluating other hallmarks of aging and their mechanisms.

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Keywords - aging, cellular senescence, heterochronic parabiosis, geroscience

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:

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Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com​​

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MEDIA@IMPACTJOURNALS.COM

Trending With Impact: Heterochronic Parabiosis, Cellular Senescence and Aging

Oncoscience published this trending research perspective in Volume 9, 2022, entitled, "Altos Labs and the quest for immortality: but can we live longer right now?" by Dr. Mikhail V. Blagosklonny from Roswell Park Cancer Institute, Buffalo, NY. 

DOI - https://doi.org/10.18632/oncoscience.552

Corresponding author - Mikhail V. Blagosklonny - Blagosklonny@oncotarget.com, Blagosklonny@rapalogs.com

Abstract

Some visionaries prefer to dream of immortality rather than to actually live longer. 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.

Press release - https://aging-us.com/news_room/altos-labs-quest-for-immortality

Keywords - aging, longevity, lifespan, geroscience, rapalogs, gerostatics

About Oncoscience

Oncoscience's mission is to cover the rapidly growing field of cancer research. It’s aim is to focus on emergent topics not currently covered by other journals.

Launched in 2014, Oncoscience is a peer-reviewed, traditional-style, bi-monthly journal with free access. Oncoscience also has a special mission: freeing researchers in oncology from publication costs. It is free for both readers and authors.

Please visit our website at http://www.Oncoscience.us​ and connect with us:

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Oncoscience is published by Impact Journals, LLC: http://www.ImpactJournals.com​​

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Paper Spotlight: Altos Labs’ Quest for Immortality - Dr. Blagosklonny’s Perspective

Aging (Aging-US) published this trending editorial in Volume 14, Issue 8, entitled, “SNCA-AS1 in aging and Parkinson’s disease” by researchers from the Pediatric Research Center “Romeo ed Enrica Invernizzi”, Department of Biomedical and Clinical Sciences "L. Sacco", University of Milano, Milano, Italy; Department of Women, Mothers and Neonatal Care, Children's Hospital "V. Buzzi", Milano, Italy.

DOI - https://doi.org/10.18632/aging.204025

Corresponding author - Stephana Carelli - stephana.carelli@unimi.it

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Keywords - aging, SNCA-AS1, alpha-synuclein, SNCA, long non-coding RNA, Parkinson's disease

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:

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YouTube - https://www.youtube.com/agingus​
LinkedIn - https://www.linkedin.com/company/aging/
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Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com​​

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MEDIA@IMPACTJOURNALS.COM

Trending With Impact: SNCA-AS1 in Aging and Parkinson’s Disease

Aging (Aging-US) published this research paper 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" by researchers the Department of Microbiology and Immunology, Brody School of Medicine at East Carolina University, Greenville, NC; Department of Biomedical and Neuromotor Sciences, Università di Bologna, Bologna, Italy; Department of Medicine and Surgery, Re.Mo.Bio.S. Laboratory, Anatomy Section, University of Parma, Parma, Italy; Department of Molecular Physiology and Neurobiology, University of Wroclaw, Wroclaw, Poland.

DOI - https://doi.org/10.18632/aging.204038

Corresponding author - James A. McCubrey - mccubreyj@ecu.edu

Abstract

TP53 is a master regulator of many signaling and apoptotic pathways involved in: aging, cell cycle progression, gene regulation, growth, apoptosis, cellular senescence, DNA repair, drug resistance, malignant transformation, metastasis, and metabolism. Most pancreatic cancers are classified as pancreatic ductal adenocarcinomas (PDAC). The tumor suppressor gene TP53 is mutated frequently (50–75%) in PDAC. Different types of TP53 mutations have been observed including gain of function (GOF) point mutations and various deletions of the TP53 gene resulting in lack of the protein expression. Most PDACs have point mutations at the KRAS gene which result in constitutive activation of KRas and multiple downstream signaling pathways. It has been difficult to develop specific KRas inhibitors and/or methods that result in recovery of functional TP53 activity. To further elucidate the roles of TP53 in drug-resistance of pancreatic cancer cells, we introduced wild-type (WT) TP53 or a control vector into two different PDAC cell lines. Introduction of WT-TP53 increased the sensitivity of the cells to multiple chemotherapeutic drugs, signal transduction inhibitors, drugs and nutraceuticals and influenced key metabolic properties of the cells. Therefore, TP53 is a key molecule which is critical in drug sensitivity and metabolism of PDAC.

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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

Paper Spotlight: Restoration of Wild-Type TP53 in Pancreatic Cancer

Aging (Aging-US) published this trending research paper in Volume 14, Issue 7, entitled, “The tobacco phosphatidylethanolamine-binding protein NtFT4 increases the lifespan of Drosophila melanogaster by interacting with the proteostasis network” by researchers from the Fraunhofer Institute for Molecular Biology and Applied Ecology IME, Münster, Germany; Institute of Plant Biology and Biotechnology, University of Münster, Münster, Germany; Institute of Neuro- and Behavioral Biology, University of Münster, Münster, Germany; TRM Ltd, Scarborough, United Kingdom.

DOI - https://doi.org/10.18632/aging.204005

Corresponding author - Philip Känel - philip.kaenel@ime.fraunhofer.de

Abstract
Proteostasis reflects the well-balanced synthesis, trafficking and degradation of cellular proteins. This is a fundamental aspect of the dynamic cellular proteome, which integrates multiple signaling pathways, but it becomes increasingly error-prone during aging. Phosphatidylethanolamine-binding proteins (PEBPs) are highly conserved regulators of signaling networks and could therefore affect aging-related processes. To test this hypothesis, we expressed PEPBs in a heterologous context to determine their ectopic activity. We found that heterologous expression of the tobacco (Nicotiana tabacum) PEBP NtFT4 in Drosophila melanogaster significantly increased the lifespan of adult flies and reduced age-related locomotor decline. Similarly, overexpression of the Drosophila ortholog CG7054 increased longevity, whereas its suppression by RNA interference had the opposite effect. In tobacco, NtFT4 acts as a floral regulator by integrating environmental and intrinsic stimuli to promote the transition to reproductive growth. In Drosophila, NtFT4 engaged distinct targets related to proteostasis, such as HSP26. In older flies, it also prolonged Hsp26 gene expression, which promotes longevity by maintaining protein integrity. In NtFT4-transgenic flies, we identified deregulated genes encoding proteases that may contribute to proteome stability at equilibrium. Our results demonstrate that the expression of NtFT4 influences multiple aspects of the proteome maintenance system via both physical interactions and transcriptional regulation, potentially explaining the aging-related phenotypes we observed.

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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

Aging (Aging-US)

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