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Geroscience: Linking Aging to Chronic Disease
Open accessAbstract
Mammalian aging can be delayed with genetic, dietary, and pharmacologic approaches. Given that the elderly population is dramatically increasing and that aging is the greatest risk factor for a majority of chronic diseases driving both morbidity and mortality, it is critical to expand geroscience research directed at extending human healthspan.
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“Chronological age is the major predictor for most of the diseases that account for the bulk of morbidity, mortality and health costs across low-, middle- and high-income countries2–7.”
From Cellular senescence and senolytics: the path to the clinic (2022) · cites this paper as [3]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“The Geroscience Hypothesis holds that these pillars of aging, including cellular senescence, tend to progress in concert and may be root-cause contributors to the pathophysiology of multiple diseases”
From Cellular senescence and senolytics: the path to the clinic (2022) · cites this paper as [3]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Old age is the greatest risk factor for the chronic diseases responsible for the majority of morbidity, mortality, and health-care costs worldwide (1, 2).”
From Senolytic Drugs: Reducing Senescent Cell Viability to Extend Health Span (2021) · cites this paper as [1]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Recent studies of animal models have established the veracity of the geroscience hypothesis (1).”
From Senolytic Drugs: Reducing Senescent Cell Viability to Extend Health Span (2021) · cites this paper as [1]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Interlinked and fundamental aging processes appear to be a root-cause contributor to many disorders and diseases.”
From Cellular senescence and senolytics: the path to the clinic (2022) · cites this paper as [3]
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“The recognition that old age is the greatest risk factor for most chronic diseases led to the geroscience hypothesis, which posits that therapeutically targeting fundamental aging mechanisms will successfully impact multiple chronic diseases because these diseases all share the same underlying mechanism (1).”
From Senolytic Drugs: Reducing Senescent Cell Viability to Extend Health Span (2021) · cites this paper as [1]
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“This hypothesis posits that by targeting a fundamental ageing process such as cellular senescence, multiple age-related disorders can be delayed, prevented, or alleviated as a group, instead of one-at-a-time.”
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In the citing paper
“The geroscience hypothesis proposes that therapy to slow or reverse molecular changes that occur with aging can delay or prevent multiple chronic diseases and extend healthy lifespan1–3.”
From Effect of long-term caloric restriction on DNA methylation measures of biological aging in healthy adults from the CALERIE trial (2023) · cites this paper as [2]
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“Evidence amassed in recent years indicates that aging science shows great promise as a method of extending health span (50)(51)(52)(53)(54)(55)(56).”
From Inconvenient Truths About Human Longevity (2019) · cites this paper as [51]
In the citing paper
“The somewhat surprising finding is that DNA damage has far-reaching effects on many aspects of cellular metabolism tied to aging, the so-called pillars of aging (Kennedy et al., 2014).”
From DNA damage-how and why we age? (2021) · cites this paper as Kennedy et al., 2014
In the citing paper
“Senescent cells expressing this phenotype can in turn promote a multitude of chronic health conditions and diseases, including insulin resistance, CVD, pulmonary arterial hypertension, chronic obstructive pulmonary disorder, emphysema, Alzheimer’s and Parkinson’s diseases, macular degeneration, osteoarthritis and cancer54,55.”
From Chronic inflammation in the etiology of disease across the life span (2019) · cites this paper as [55]
In the citing paper
“Paramount among them is the accumulation of senescent cells in multiple tissues.”
From Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty (2018) · cites this paper as [87]
In the citing paper
“Thus, PA and exercise may be considered central geriatric care interventions, that is, interventions that act on the cellular and molecular drivers of biological aging to decelerate the rates of aging, which constitute the basics of the geroscience field [633,634].”
From Global consensus on optimal exercise recommendations for enhancing healthy longevity in older adults (ICFSR) (2025) · cites this paper as [634]
In the citing paper
“Thus, PA and exercise may be considered central geriatric care interventions, that is, interventions that act on the cellular and molecular drivers of biological aging to decelerate the rates of aging, which constitute the basics of the geroscience field [633,634].”
From Global consensus on optimal exercise recommendations for enhancing healthy longevity in older adults (ICFSR) (2025) · cites this paper as [634]
In the citing paper
“The hallmarks of aging are interconnected (Kennedy et al., 2014; López-Otín et al., 2013; Zhang et al., 2015a), and age-associated perturbations of one can affect others.”
From The Aging Epigenome (2016) · cites this paper as Kennedy et al., 2014
In the citing paper
“Over the past decades, a large body of research has shown that the molecular and cellular decline of aging can be organized into several evolutionarily conserved hallmarks or pillars of aging (Kennedy et al., 2014; López-Otín et al., 2013).”
From The Aging Epigenome (2016) · cites this paper as Kennedy et al., 2014
In the citing paper
“time‐dependent loss of autophagy proficiency is thought to critically contribute to the aged phenotype (Lopez‐Otin et al, 2013; Kennedy et al, 2014; Lopez‐Otin & Kroemer, 2021)”
From Autophagy in major human diseases (2021) · cites this paper as Kennedy et al, 2014
In the citing paper
“The molecular causes of physical aging are thought to occur through the accumulation of cellular damage to mitochondrial DNA (mtDNA), telomeric ends, coding-DNA, and proteins (Kennedy et al, 2014).”
From Sleep health: Reciprocal regulation of sleep and innate immunity (2017) · cites this paper as Kennedy et al, 2014
In the citing paper
“Ageing is also characterized by the appearance of different chronic diseases such as sarcopenia, type 2 diabetes mellitus (T2DM), cardiovascular disease, hypercholesterolemia, hypertension or neurodegenerative diseases among others (Kennedy et al., 2014).”
From Mitochondrial Activity and Dynamics Changes Regarding Metabolism in Ageing and Obesity (2017) · cites this paper as Kennedy et al., 2014
In the citing paper
“Ageing is multifactorial involving different molecular and cellular processes such as genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intracellular communication (Kennedy et al., 2014; Lopez-Otin et al., 2013).”
From Mitochondrial Activity and Dynamics Changes Regarding Metabolism in Ageing and Obesity (2017) · cites this paper as Kennedy et al., 2014
In the citing paper
“The geroscience hypothesis posits that interventions that target key hallmarks of aging potentially can prevent, delay, or even reverse age-related conditions as a group (1).”
From Exercise Counters the Age-Related Accumulation of Senescent Cells (2022) · cites this paper as [1]
In the citing paper
“Biological ageing is enormously complex and is thought to be driven by the interaction of multiple dysregulated cellular and biochemical processes3,4.”
From Measuring biological age using omics data (2022) · cites this paper as [3]
In the citing paper
“Indeed, it could be argued that, as much of the basic biology of ageing seems largely conserved among many species with very different lifespans3,4,8, clocks that measure a universal cause or rate of ageing should function ubiquitously.”
From Measuring biological age using omics data (2022) · cites this paper as [3]
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Cognitive frailty: A comprehensive clinical paradigm beyond cognitive decline
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Aging mechanisms—A perspective mostly from Drosophila
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Sex differences and aging: Is there a role of brown adipose tissue?
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Post-GWAS functional analysis identifies CUX1 as a regulator of p16INK4a and cellular senescence
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Aging of enteric neuromuscular systems in gastrointestinal tract
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Canine Geriatric Syndrome: A Framework for Advancing Research in Veterinary Geroscience
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Improving intestinal inflammaging to delay aging? A new perspective
Zhang, L., Yan, J., Zhang, C., Feng, S., Zhan, Z., Bao, Y., Zhan, Z., & Chao, G. (2023) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2023.111841 · Cited by 27
Translational geroscience: From invertebrate models to companion animal and human interventions
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Effects of treadmill exercise on the regulation of tight junction proteins in aged mice
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Spatio-temporal mapping of breast and prostate cancers in South Iran from 2014 to 2017
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Association of Treatable Health Conditions During Adolescence With Accelerated Aging at Midlife
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The DNA damage response - from cell biology to human disease
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Geroscience approaches to increase healthspan and slow aging
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Whole Blood Gene Expression Associated With Clinical Biological Age
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Diet Quality and Epigenetic Aging in the Women’s Health Initiative
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Metadata
- Authors
- Kennedy, B. K., Berger, S. L., Brunet, A., Campisi, J., Cuervo, A. M., Epel, E. S., Franceschi, C., Lithgow, G. J., Morimoto, R. I., Pessin, J. E., Rando, T. A., Richardson, A., Schadt, E. E., Wyss-Coray, T., & Sierra, F.
- Affiliations
- Buck Institute for Research on Aging (US)
- University of Pennsylvania (US)
- Stanford University (US)
- University of California, San Francisco (US)
- Institute of Neurological Sciences (IT)
- Northwestern University (US)
- Albert Einstein College of Medicine (US)
- VA Palo Alto Health Care System (US)
- Oklahoma City VA Medical Center (US)
- Icahn School of Medicine at Mount Sinai (US)
- National Institutes of Health (US)
- Corresponding author
- Kennedy, Brian K.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2014-11
- Volume
- 159
- Issue
- 4
- Pages
- 709-713
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC4852871
- OpenAlex
- W2159914115
- Cited by
- 2,764
- References
- 15
- Citations by year
- 2026: 368 · 2025: 355 · 2024: 344 · 2023: 272 · 2022: 296 · 2021: 313 · 2020: 244 · 2019: 187 · 2018: 150 · 2017: 105 · 2016: 81 · 2015: 42 · 2014: 3
- FWCI
- 26.34
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (R01AG043080, R01AG033373, P01AG031782, R01AG024287, P01AG036695)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
- Keywords
- geroscience, aging, chronic disease, healthspan extension, aging interventions, dietary intervention, older adults
- MeSH terms
- Aging, Animals, Chronic Disease, Humans, Biomedical Research, Epigenesis, Genetic, Gene-Environment Interaction
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