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 (Aging-US) published this priority research paper as the cover for Volume 14, Issue 1, entitled, "Reduced growth rate of aged muscle stem cells is associated with impaired mechanosensitivity" by researchers from the Laboratory for Myology, Department of Human Movement Sciences, Faculty of Behavioural and Movement Sciences, Vrije Universiteit Amsterdam, Amsterdam Movement Sciences, Amsterdam 1081 HZ, The Netherlands; Department of Oral Cell Biology, Academic Centre for Dentistry Amsterdam, University of Amsterdam and Vrije Universiteit Amsterdam, Amsterdam Movement Sciences, Amsterdam 1081 LA, The Netherlands; Sorbonne Université, INSERM UMRS974, Center for Research in Myology, Paris 75013, France; Department of Physiology, Amsterdam University Medical Center VUmc, Amsterdam Cardiovascular Sciences, Amsterdam 1081 HZ, The Netherlands; Institute of Neuroscience, Université Catholique de Louvain, Louvain-la-Neuve 1348, Belgium; Exercise Physiology Research Group, Department of Movement Sciences, KU Leuven, Leuven 3001, Belgium; Faculty of Medicine and Pharmacy, NeuroMyoGène UCBL-CNRS UMR 5310, INSERM U1217, Lyon 69008, France.

DOI - https://doi.org/10.18632/aging.203830

Correspondence to - Richard T. Jaspers - r.t.jaspers@vu.nl

Abstract:
Aging-associated muscle wasting and impaired regeneration are caused by deficiencies in muscle stem cell (MuSC) number and function. We postulated that aged MuSCs are intrinsically impaired in their responsiveness to omnipresent mechanical cues through alterations in MuSC morphology, mechanical properties, and number of integrins, culminating in impaired proliferative capacity. Here we show that aged MuSCs exhibited significantly lower growth rate and reduced integrin-α7 expression as well as lower number of phospho-paxillin clusters than young MuSCs. Moreover, aged MuSCs were less firmly attached to matrigel-coated glass substrates compared to young MuSCs, as 43% of the cells detached in response to pulsating fluid shear stress (1 Pa). YAP nuclear localization was 59% higher than in young MuSCs, yet YAP target genes Cyr61 and Ctgf were substantially downregulated. When subjected to pulsating fluid shear stress, aged MuSCs exhibited reduced upregulation of proliferation-related genes. Together these results indicate that aged MuSCs exhibit impaired mechanosensitivity and growth potential, accompanied by altered morphology and mechanical properties as well as reduced integrin-α7 expression. Aging-associated impaired muscle regenerative capacity and muscle wasting is likely due to aging-induced intrinsic MuSC alterations and dysfunctional mechanosensitivity.

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Keywords - aging, mechanosensitivity, muscle stem cell, proliferation, YAP signaling

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:

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

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Impaired Mechanosensitivity in Aged Muscle Stem Cells

Aging (Aging-US) published this research paper in Volume 11, Issue 18, entitled, "Inadequate control of thyroid hormones sensitizes to hepatocarcinogenesis and unhealthy aging" by researchers from the Department of Regeneration and Cell Therapy, Andalusian Center for Molecular Biology and Regenerative Medicine-CABIMER, Junta de Andalucia-University of Pablo de Olavide-University of Seville-CSIC, Seville, Spain; Instituto de la Grasa (CSIC), Universidad Pablo de Olavide, Sevilla, Spain; Centro de Investigación Príncipe Felipe, Valencia, Spain; Department of Human Physiology, Málaga University, Biomedical Research Institute of Málaga (IBIMA), Málaga, Spain; Instituto de Investigación Biomédica de Málaga-IBIMA, UGC Endocrinología y Nutrición. Hospital Regional Universitario de Málaga, Málaga, Spain; Biomedical Research Network on Diabetes and Related Metabolic Diseases-CIBERDEM, Instituto de Salud Carlos III, Madrid, Spain; Centro Andaluz de Biología del Desarrollo, Universidad Pablo de Olavide and CIBERER, Sevilla, Spain; Department of Physiology, University Miguel Hernández School of Medicine Sant Joan d'Alacant, Alicante, Spain.

DOI - https://doi.org/10.18632/aging.102285

Correspondence to - Alejandro Martin-Montalvo - alejandro.martinmontalvo@cabimer.es and Benoit Raymond Gauthier - benoit.gauthier@cabimer.es

Abstract:
An inverse correlation between thyroid hormone levels and longevity has been reported in several species and reduced thyroid hormone levels have been proposed as a biomarker for healthy aging and metabolic fitness. However, hypothyroidism is a medical condition associated with compromised health and reduced life expectancy. Herein, we show, using wild-type and the Pax8 ablated model of hypothyroidism in mice, that hyperthyroidism and severe hypothyroidism are associated with an overall unhealthy status and shorter lifespan. Mild hypothyroid Pax8 +/- mice were heavier and displayed insulin resistance, hepatic steatosis and increased prevalence of liver cancer yet had normal lifespan. These pathophysiological conditions were precipitated by hepatic mitochondrial dysfunction and oxidative damage accumulation. These findings indicate that individuals carrying mutations on PAX8 may be susceptible to develop liver cancer and/or diabetes and raise concerns regarding the development of interventions aiming to modulate thyroid hormones to promote healthy aging or lifespan in mammals.

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Press release - https://www.aging-us.com/news_room/inadequate-control-of-thyroid-hormones-sensitizes-to-hepatocarcinogenesis-and-unhealthy-aging

Keywords - lifespan, healthspan, thyroid hormones, hyperthyroidism, hypothyroidism, glucose metabolism

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:

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

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MEDIA@IMPACTJOURNALS.COM

Paper Spotlight: Modulation of Thyroid Hormones Leads to Unhealthy Aging

Aging (Aging-US) published this trending research paper in Volume 13, Issue 24, entitled, "Maternal adverse childhood experiences before pregnancy are associated with epigenetic aging changes in their children" by researchers from the Gangarosa Department of Environmental Health, Emory Rollins School of Public Health, Atlanta, GA; Department of Emergency Medicine, Emory University School of Medicine, Atlanta, GA; Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, CA; Center for Computational Biology, School of Public Health, University of California, Berkeley, CA; Center for Environmental Research of Community Health, CERCH, School of Public Health, University of California, Berkeley, CA; Community Health Sciences Division, School of Public Health, University of California, Berkeley, CA.

Abstract:
Emerging research suggests associations of physical and psychosocial stressors with epigenetic aging. Although this work has included early-life exposures, data on maternal exposures and epigenetic aging of their children remain sparse. Using longitudinally collected data from the California, Salinas Valley CHAMACOS study, we examined relationships between maternal Adverse Childhood Experiences (ACEs) reported up to 18 years of life, prior to pregnancy, with eight measures (Horvath, Hannum, SkinBloodClock, Intrinsic, Extrinsic, PhenoAge, GrimAge, and DNAm telomere length) of blood leukocyte epigenetic age acceleration (EAA) in their children at ages 7, 9, and 14 years (N = 238 participants with 483 observations). After adjusting for maternal chronological age at delivery, pregnancy smoking/alcohol use, parity, child gestational age, and estimated leukocyte proportions, higher maternal ACEs were significantly associated with at least a 0.76-year increase in child Horvath and Intrinsic EAA. Higher maternal ACEs were also associated with a 0.04 kb greater DNAm estimate of telomere length of children. Overall, our data suggests that maternal preconception ACEs are associated with biological aging in their offspring in childhood and that preconception ACEs have differential relationships with EAA measures, suggesting different physiologic utilities of EEA measures. Studies are necessary to confirm these findings and to elucidate potential pathways to explain these relationships, which may include intergenerational epigenetic inheritance and persistent physical and social exposomes.

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DOI - https://doi.org/10.18632/aging.203776

Full text - https://www.aging-us.com/article/203776/text

Correspondence to: Andres Cardenas email: andres.cardenas@berkeley.edu

Keywords: ACES, epigenetic age, DNA methylation, mitotic clocks, adversity

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 on:

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​
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Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com​​ or connect with @ImpactJrnls

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18009220957
MEDIA@IMPACTJOURNALS.COM

Trending With Impact: Maternal ACEs Associated With Biological Aging in Children

Aging (Aging-US) published this trending research paper in Volume 11, Issue 24, entitled, "Age-related changes in eye lens biomechanics, morphology, refractive index and transparency" by researchers from the School of Optometry, Indiana University, Bloomington, IN; Department of Molecular Medicine, The Scripps Research Institute, La Jolla, CA; Department of Biological Sciences, University of Delaware, Newark, DE; Department of Neurobiology, Morehouse School of Medicine, Atlanta, GA; School of Science and Technology, Nottingham Trent University, Nottingham, United Kingdom; Japan Synchrotron Radiation Research Institute (Spring-8), Sayo-cho, Sayo-gun, Hyogo, Japan; Department of Radiology, Boston University School of Medicine, Boston, MA.

Abstract:
Life-long eye lens function requires an appropriate gradient refractive index, biomechanical integrity and transparency. We conducted an extensive study of wild-type mouse lenses 1-30 months of age to define common age-related changes. Biomechanical testing and morphometrics revealed an increase in lens volume and stiffness with age. Lens capsule thickness and peripheral fiber cell widths increased between 2 to 4 months of age but not further, and thus, cannot account for significant age-dependent increases in lens stiffness after 4 months. In lenses from mice older than 12 months, we routinely observed cataracts due to changes in cell structure, with anterior cataracts due to incomplete suture closure and a cortical ring cataract corresponding to a zone of compaction in cortical lens fiber cells. Refractive index measurements showed a rapid growth in peak refractive index between 1 to 6 months of age, and the area of highest refractive index is correlated with increases in lens nucleus size with age. These data provide a comprehensive overview of age-related changes in murine lenses, including lens size, stiffness, nuclear fraction, refractive index, transparency, capsule thickness and cell structure. Our results suggest similarities between murine and primate lenses and provide a baseline for future lens aging studies.

Special collection on eye disease - https://www.aging-us.com/special-collections-archive/eye-disease

Press release - https://www.aging-us.com/news_room/age-related-changes-in-eye-lens-biomechanics

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DOI - https://doi.org/10.18632/aging.102584

Full text - https://www.aging-us.com/article/102584/text

Correspondence to: Velia M. Fowler email: vfowler@udel.edu and Catherine Cheng email: ckcheng@iu.edu

Keywords: fiber cell, strain, epithelial cell, cataract, stiffness

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 on:

SoundCloud - https://soundcloud.com/Aging-Us
Facebook - https://www.facebook.com/AgingUS/
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YouTube - https://www.youtube.com/agingus​
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Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com​​ or connect with @ImpactJrnls

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Paper Spotlight: Common Age-related Changes in Eye Lens Function

Copy: Aging-US published this research paper as the cover for Volume 13, Issue 24, entitled, “Age-dependent expression changes of circadian system-related genes reveal a potentially conserved link to aging” by researchers from Bioinformatics/High Throughput Analysis, Faculty of Mathematics and Computer Science, Friedrich Schiller University Jena, Jena, Germany; FLI Leibniz Institute for Age Research, Jena, Germany; Hans Berger Department of Neurology, Jena University Hospital, Jena, Germany; German Center for Integrative Biodiversity Research (iDiv), Halle-Jena-Leipzig, Germany; European Virus Bioinformatics Center (EVBC), Jena, Germany.

Abstract
The circadian clock system influences the biology of life by establishing circadian rhythms in organisms, tissues, and cells, thus regulating essential biological processes based on the day/night cycle. Circadian rhythms change over a lifetime due to maturation and aging, and disturbances in the control of the circadian system are associated with several age-related pathologies.

However, the impact of chronobiology and the circadian system on healthy organ and tissue aging remains largely unknown. Whether aging-related changes of the circadian system’s regulation follow a conserved pattern across different species and tissues, hence representing a common driving force of aging, is unclear.

Based on a cross-sectional transcriptome analysis covering 329 RNA-Seq libraries, we provide indications that the circadian system is subjected to aging-related gene alterations shared between evolutionarily distinct species, such as Homo sapiens, Mus musculus, Danio rerio, and Nothobranchius furzeri. We discovered differentially expressed genes by comparing tissue-specific transcriptional profiles of mature, aged, and old-age individuals and report on six genes (per2, dec2, cirp, klf10, nfil3, and dbp) of the circadian system, which show conserved aging-related expression patterns in four organs of the species examined. Our results illustrate how the circadian system and aging might influence each other in various tissues over a long lifespan and conceptually complement previous studies tracking short-term diurnal and nocturnal gene expression oscillations.

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DOI - https://doi.org/10.18632/aging.203788

Full Text - https://www.aging-us.com/article/203788/text

Correspondence to: Emanuel Barth email: emanuel.barth@uni-jena.de

Keywords: aging, circadian clock system, circadian rhythm, inter-species comparison, longevity, RNA-Seq

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 on:

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​
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Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com​​ or connect with @ImpactJrnls

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The Circadian System and Aging

Aging-US published "DNA methylation-based measures of biological age: meta-analysis predicting time to death" in 2016, which reported that estimates of biological age based on DNA methylation patterns, often referred to as "epigenetic age", "DNAm age", have been shown to be robust biomarkers of age in humans.

These authors previously demonstrated that independent of chronological age, epigenetic age assessed in blood predicted all-cause mortality in four human cohorts. Here, they expanded their original observation to 13 different cohorts for a total sample size of 13,089 individuals, including three racial/ethnic groups. In addition, they examined whether incorporating information on blood cell composition into the epigenetic age metrics improves their predictive power for mortality.

All considered measures of epigenetic age acceleration were predictive of mortality, independent of chronological age, even after adjusting for additional risk factors.

The authors said, "DNA methylation-based biomarkers, often referred to as ‘epigenetic age’ or ‘epigenetic clock’, are robust estimators of chronological age of an individual."

This estimate is consistent across most types of biological specimens, including whole blood, brain, breast, kidney, liver, lung, and saliva and cell types, including CD4 T cells, monocytes, B cells, glial cells, and neurons.

It is well known that blood cell composition changes with age and some of these changes might be independent predictors of mortality. Thus, it is of interest to understand whether considering information on blood cell composition in measures of epigenetic age improves their predictive power for mortality.

Here, the authors evaluated the ability to predict time to death for blood-based epigenetic age measures, both published and novel measures that incorporate information on blood cell composition.

Due to the well documented age-related changes in blood cell composition, they were able to distinguish epigenetic measures of age that were independent of changes in blood cell composition, and measures that incorporated age-related changes in blood cell composition.

The Research Team concluded in their Aging-US Research Output, "our results inform the ongoing debate about whether epigenetic biomarkers of age capture an aspect of biological age. While epigenetic processes are unlikely to be the only mediators of chronological age on mortality—in fact, multiple risk factors have stronger effects on mortality—our results suggest that at least one of the mediating processes relates to the epigenetic age of blood tissue and that this process is independent of age-dependent changes in blood cell composition. Future studies will be useful for gaining a mechanistic understanding of this intrinsic epigenetic aging process."

Full Text - https://www.aging-us.com/article/101020/text/

Correspondence to: Steve Horvath email: shorvath@mednet.ucla.edu

Keywords: all-cause mortality, lifespan, epigenetics, epigenetic clock, DNA+methylation, mortality

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 on:

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 please visit http://www.ImpactJournals.com​​ or connect with @ImpactJrnls

Media Contact
18009220957
MEDIA@IMPACTJOURNALS.COM

Aging (Aging-US)

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