The Hallmarks of Aging

López-Otín, Carlos; Blasco, Maria A.; Partridge, Linda; Serrano, Manuel; Kroemer, Guido

doi:10.1016/j.cell.2013.05.039

Cited by 14,982Genetics, Aging, and Longevity in Model OrganismsTelomeres, Telomerase, and SenescenceAutophagy in Disease and Therapy

The Hallmarks of Aging

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López-Otín, Carlos, Blasco, Maria A., Partridge, Linda, Serrano, Manuel, Kroemer, Guido·2013·Cell

DOI 10.1016/j.cell.2013.05.039PMC PMC3836174

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Abstract

Aging is characterized by a progressive loss of physiological integrity, leading to impaired function and increased vulnerability to death. This deterioration is the primary risk factor for major human pathologies, including cancer, diabetes, cardiovascular disorders, and neurodegenerative diseases. Aging research has experienced an unprecedented advance over recent years, particularly with the discovery that the rate of aging is controlled, at least to some extent, by genetic pathways and biochemical processes conserved in evolution. This Review enumerates nine tentative hallmarks that represent common denominators of aging in different organisms, with special emphasis on mammalian aging. These hallmarks are: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. A major challenge is to dissect the interconnectedness between the candidate hallmarks and their relative contributions to aging, with the final goal of identifying pharmaceutical targets to improve human health during aging, with minimal side effects.

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Aging leads to dysfunctional mitochondria with defective mitophagy and bioenergetics, producing excess free radicals that damage the cellular environment.
“As we age, mitochondria become increasingly dysfunctional, with defective mitophagy and bioenergetic capabilities which end up producing excess free radicals inside the cell, damaging the global cellular environment [101].”
From NAD+ Precursors Nicotinamide Mononucleotide (NMN) and Nicotinamide Riboside (NR): Potential Dietary Contribution to Health (2023) · cites this paper as [101]
The Mitochondrial Dysfunction section describes declining respiratory-chain efficiency with age, and its Mitochondrial integrity and biogenesis subsection identifies defective mitophagy as a cause of impaired bioenergetics. The Reactive oxygen species subsection says ROS levels can rise with age and eventually aggravate cellular damage. But the paper does not present excess ROS as an inevitable result of mitochondrial dysfunction: its Genomic Instability > Mitochondrial DNA subsection reports impaired mitochondrial function without increased ROS production. (LLM, conf=0.88)
Experimental — accuracy not yet measured
Accumulated DNA damage in chromosomal regions leads to progressive and cumulative loss of protective telomere sequences at chromosome ends.
“In addition, accumulated DNA damage in chromosomal regions leads to a progressive and cumulative loss of protective telomere sequences at the chromosome end [101].”
From NAD+ Precursors Nicotinamide Mononucleotide (NMN) and Nicotinamide Riboside (NR): Potential Dietary Contribution to Health (2023) · cites this paper as [101]
The Telomere Attrition section confirms progressive, cumulative loss of protective sequences from chromosome ends. But it attributes that loss to incomplete replication of chromosome ends and the absence of telomerase in most mammalian somatic cells, not to accumulated DNA damage in chromosomal regions. It discusses damage at telomeres separately as a cause of persistent damage and deleterious cellular effects. (LLM, conf=0.87)
Experimental — accuracy not yet measured
Short telomeres show decreased expression and activity of sirtuins and marked mitochondrial dysfunction.
“Short telomeres showed decreased expression and activity of sirtuins and marked mitochondrial dysfunction.”
From NAD+ Precursors Nicotinamide Mononucleotide (NMN) and Nicotinamide Riboside (NR): Potential Dietary Contribution to Health (2023) · cites this paper as [101]
The Mitochondrial Dysfunction section links telomere attrition in telomerase-deficient mice to reduced mitochondrial biogenesis and describes mitochondrial decline. It also discusses sirtuins’ roles in mitochondrial function, but does not say that short telomeres decrease sirtuin expression or activity. The claim also presents the mitochondrial finding more broadly than the mouse-specific example in the passage. (LLM, conf=0.86)
Experimental — accuracy not yet measured
Evidence from yeast and mammals supports an Information Theory of Ageing in which loss of epigenetic information disrupts youthful gene expression, causing cellular dysfunction and senescence.
“Evidence from yeast and mammals supports an Information Theory of Ageing10,11, in which the loss of epigenetic information disrupts youthful gene expression patterns1–3, leading to cellular dysfunction and senescence12,13.”
From Reprogramming to recover youthful epigenetic information and restore vision (2020) · cites this paper as [12]
The Epigenetic Alterations overview (page not provided) says aging is accompanied by epigenetic changes, and the Transcriptional alterations section reports age-related changes in gene expression. The paper also discusses longevity-related evidence from yeast and mammals. It does not set out an Information Theory of Ageing or establish the claimed causal chain from loss of epigenetic information through disrupted youthful expression to cellular dysfunction and senescence. (LLM, conf=0.85)
Experimental — accuracy not yet measured
Old age is the strongest risk factor for the chronic diseases that account for most morbidity, mortality, and health-care costs globally.
“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 [2]
The indexed Abstract (page not provided) calls aging the primary risk factor for major human pathologies, including cancer, diabetes, cardiovascular disorders, and neurodegenerative diseases. It does not say that these diseases account for the majority of morbidity, mortality, and health-care costs worldwide. (LLM, conf=0.88)
Experimental — accuracy not yet measured

Telomeres shorten with each cell division, so average telomere length declines continuously across life.
“Telomeres, protective caps at the ends of chromosomes, shorten with each cell division, resulting in continual decline in average telomere length (TL) across the lifespan (López-Otín et al., 2013).”
From Telomere trajectories from early adolescence to adulthood following early institutionalization: Protective effects of foster care in the Bucharest Early Intervention Project (2026) · cites this paper as López-Otín et al., 2013
The Telomere Attrition section says most mammalian somatic cells lack telomerase, leading to progressive, cumulative loss of telomere-protective sequences, and that shortening occurs during normal aging. It does not establish that telomeres shorten with every cell division in all cells or that average telomere length declines continuously across the entire lifespan. (LLM, conf=0.82)
Experimental — accuracy not yet measured
Aged or stressed microglia present a buildup of intracellular LDs, deterioration of mitochondrial efficiency, and downregulation of oxidative phosphorylation-related genes.
“aged or stressed microglia present a buildup of intracellular LDs, deterioration of mitochondrial efficiency, and downregulation of oxidative phosphorylation-related genes [59, 60].”
From The protective PLCγ2-P522R variant mitigates Alzheimer’s disease-associated pathologies by enhancing beneficial microglial functions (2025) · cites this paper as [60]
The Mitochondrial Dysfunction section (page not provided) says that respiratory-chain efficiency tends to diminish with age, supporting the general point about declining mitochondrial efficiency. It does not establish that this occurs specifically in aged or stressed microglia, or report intracellular lipid-droplet buildup or downregulation of oxidative-phosphorylation-related genes in those cells. (LLM, conf=0.86)
Experimental — accuracy not yet measured
Ageing is marked by altered cell-to-cell communication that contributes to progressive functional decline.
“This complexity becomes especially evident during ageing, a process marked by altered CCC that contributes to progressive functional decline [6].”
From Quantitative profiling of lifespan-dependent cell-cell communication potential reveals dynamic ligand-receptor network shifts across mouse tissues (2026) · cites this paper as [6]
Interlinked fundamental aging processes appear to act as root causes of many disorders and diseases.
“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 [15]
The Geroscience Hypothesis holds that the pillars of aging, including cellular senescence, tend to progress together and may be root-cause contributors to multiple diseases, age-related dysfunction, and loss of resilience.
“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 [15]
Our results confirm that TL declines with age, supporting its role as a marker of cellular aging.
“In line with prior studies, our results confirm that TL declines with age, supporting its role as a marker of cellular aging (López-Otín et al., 2013).”
From Telomere trajectories from early adolescence to adulthood following early institutionalization: Protective effects of foster care in the Bucharest Early Intervention Project (2026) · cites this paper as López-Otín et al., 2013
Aging is associated with extensive remodeling of the epigenome.
“Aging is associated with extensive remodeling of the epigenome54.”
From The role of retrotransposable elements in ageing and age-associated diseases (2021) · cites this paper as [54]
Cellular senescence is a central hallmark of aging.
“Cellular senescence, a central hallmark of aging,13,14”
From Uncovering the signatures of aging and senescence in the human dorsolateral prefrontal cortex (2026) · cites this paper as [14]
Aging is a slow process of deterioration of various homeostatic functions accompanied by an increased prevalence of disease.
“Aging is a slow process of deterioration of various homeostatic functions accompanied by an increased prevalence of disease”
From The Microbiota-Gut-Brain Axis (2019) · cites this paper as Lopez-Otin et al., 2013
Genome wide expression profiling studies have identified several genes and biological pathways affected by aging.
“Genome wide expression profiling studies have identified several genes and biological pathways affected by aging (Bishop et al. 2010, Lopez-Otin et al. 2013, Kenyon 2010, Yankner et al. 2008).”
From miR‐186 is decreased in aged brain and suppresses <scp>BACE</scp>1 expression (2016) · cites this paper as Lopez-Otin et al. 2013
There are several hypermorphic variants in PLCG2 that have been associated with autoimmune disease and cancer.
“There are several hypermorphic variants in PLCG2 that have been associated with autoimmune disease and cancer [58–61, 66].”
From The protective PLCγ2-P522R variant mitigates Alzheimer’s disease-associated pathologies by enhancing beneficial microglial functions (2025) · cites this paper as [60]
The retrieved Genomic Instability > Nuclear architecture passage discusses LMNA mutations and premature aging, not PLCG2. Searches for PLCG2 hypermorphic variants and phospholipase C gamma 2 gain-of-function variants found no passage in our copy linking them to autoimmune disease or cancer. (LLM, conf=0.76)
Experimental — accuracy not yet measured
Biological aging is driven by conserved molecular mechanisms that can be targeted and are summarized as the hallmarks of aging.
“Biological aging involves an interplay of conserved and targetable molecular mechanisms, summarized as the hallmarks of aging.”
From Benefits of Metformin in Attenuating the Hallmarks of Aging (2020) · cites this paper as López-Otín et al. 2013
Aging and age-related diseases upregulate mTORC1, while AMPK and sirtuins act in the opposite direction to mTOR signaling.
“aging and age-related diseases upregulate mTORC1, while AMPK and sirtuins act in the opposite direction to mTOR signaling”
From Benefits of Metformin in Attenuating the Hallmarks of Aging (2020) · cites this paper as López-Otín et al. 2013
The most important nutrient sensors and signaling cascades regulating aging and longevity include the GH/IGF-1 somatotropic axis, mTOR, AMPK, and sirtuins.
“These include highly conserved nutrient-sensing systems- 1) Somatotropic axis (GH/IGF-1) that elicits a response similar to insulin, regarding the cellular availability of glucose; 2) mTOR signaling responsible for sensing high amino acid concentrations; 3) AMPK that is involved in sensing low energy states via high AMP levels; 4) Sirtuins that complement in sensing low energy states by detecting”
From Benefits of Metformin in Attenuating the Hallmarks of Aging (2020) · cites this paper as López-Otín et al. 2013
A key consequence of disrupted intercellular communication is inflammaging, accompanied by increased pro-inflammatory cytokines (TNF, IL-6, IL-1beta), NF-kB and interferon signaling, senescent cell burden and secretome, and altered autophagy.
“A key consequence of this dysregulation is age-associated chronic, sterile, low-grade inflammatory state called inflammaging, that is usually accompanied by a consistent increase in pro-inflammatory cytokine secretion (TNF, IL-6, and IL-1β), activation of NF-κB and interferon signaling, increased burden of senescent cells and their secretome as well as altered autophagic response”
From Benefits of Metformin in Attenuating the Hallmarks of Aging (2020) · cites this paper as López-Otín et al. 2013
Aging leads to systemic dysregulation of cell-cell connectivity and associated responses, disrupting intercellular communication.
“Aging leads to a systemic dysregulation of effective cell-cell connectivity and its associated response disrupting the maintenance of intercellular communication.”
From Benefits of Metformin in Attenuating the Hallmarks of Aging (2020) · cites this paper as López-Otín et al. 2013
Aging-induced disruptions in mitochondrial function result from stresses including mtDNA mutations, nuclear genomic instability, reduced mitochondrial biogenesis, defective mitophagy, and altered mitochondrial dynamics and ETC regulation.
“Aging induced disruptions in mitochondrial function is a result of several intra- and extracellular stresses including mtDNA mutations, nuclear genomic instability, reduced mitochondrial biogenesis, defective mitophagy, and altered mitochondrial dynamics and ETC regulation”
From Benefits of Metformin in Attenuating the Hallmarks of Aging (2020) · cites this paper as López-Otín et al. 2013
Maintaining homeostasis of stem and progenitor cells and their regeneration potential is imperative because both reduced stem cell number and excessive proliferation can induce aging phenotypes.
“It is imperative to maintain homeostasis of stem and progenitor cells and their regeneration potential since both a reduced number of stem cells and excessive proliferation can induce aging phenotypes”
From Benefits of Metformin in Attenuating the Hallmarks of Aging (2020) · cites this paper as López-Otín et al. 2013
Diabetes may be caused in part by a convergence of basic aging mechanisms, including chronic sterile inflammation, macromolecular damage, progenitor cell dysfunction, and cellular senescence.
“Like other age-related chronic diseases, diabetes may be caused in part by a convergence of the basic aging mechanisms that underlie age-related tissue dysfunction, including chronic “sterile” (not pathogen-associated) inflammation, macromolecular damage, progenitor cell dysfunction, and cellular senescence (8).”
From Cellular Senescence in Type 2 Diabetes: A Therapeutic Opportunity (2015) · cites this paper as [8]
Cellular senescence is a process that globally regulates cell fate and can be considered a hallmark of aging.
“Cellular senescence, a seminal discovery of Hayflick and Moorhead (1961) is a process that globally regulates cell fate and can be considered a hallmark of aging (Hayflick and Moorhead, 1961; López-Otín et al., 2013).”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as López-Otín et al., 2013
Senescence itself can drive aging and is one of its key hallmarks.
“subsequent discoveries have demonstrated the presence of senescent cells in vivo and an increase in their number with age supporting the hypothesis that senescence itself can drive aging and is one of its key hallmarks (Hayflick and Moorhead, 1961; Hayflick, 1965; López-Otín et al., 2013).”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as López-Otín et al., 2013
Accumulation of senescent cells as organisms age is thought to promote aging-related phenotypes and diseases, including cancer and neurodegeneration, in a cell-nonautonomous manner.
“the accumulation of senescent cells as organisms age is thought to promote aging-related phenotypes and aging-associated diseases, including cancer and neurodegeneration, in a cell-nonautonomous manner (2, 3, 10).”
From The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4. (2015) · cites this paper as [3]
Senescent cells accumulate during organismal aging due to increased generation and inefficient clearance.
“Mounting evidence, however, indicates that senescent cells accumulate during organismal aging due to their increased generation coupled to inefficient clearance [935, 941, 960, 961].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [960]
Genomic instability, telomere attrition, loss of proteostasis, dysregulated nutrient sensing, mitochondrial dysfunction, stem cell exhaustion, altered cellular communication and excessive cellular senescence are hallmarks of ageing.
“Genomic instability, telomere attrition, loss of proteostasis, dysregulated nutrient sensing, mitochondrial dysfunction, stem cell exhaustion, altered cellular communication and excessive cellular senescence have all been recognized as hallmarks of ageing [14].”
From Ageing, Cellular Senescence and Neurodegenerative Disease (2018) · cites this paper as [14]
Random irreparable ROS-mediated damage to the DNA of cells and mitochondrial dysfunction are strong inducers of cellular senescence.
“Random irreparable ROS-mediated damage to the DNA of cells and mitochondrial dysfunction are strong inducers of cellular senescence [14].”
From Ageing, Cellular Senescence and Neurodegenerative Disease (2018) · cites this paper as [14]
Cellular senescence is an age-dependent process known to be accelerated by oxidative stress and chronic inflammation.
“Cellular senescence is an age-dependent process known to be accelerated by oxidative stress and chronic inflammation [14,20].”
From Ageing, Cellular Senescence and Neurodegenerative Disease (2018) · cites this paper as [14]
Accumulation of senescent cells with time is a cause of aging.
“Experimental evidence points to this accumulation of senescent cells with time as a cause of aging6,7.”
From Identification and characterization of Cardiac Glycosides as senolytic compounds (2019) · cites this paper as [7]
Accumulation of senescent cells in multiple tissues is a paramount mechanism that might account for inflammageing.
“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 [86]
With advanced age, senescent cell loads increase in different tissues throughout the body, including the brain.
“With advanced age, senescent cell loads increase in different tissues throughout the body, including the brain. 34”
From Senescence, brain inflammation, and oligomeric tau drive cognitive decline in Alzheimer's disease: Evidence from clinical and preclinical studies (2024) · cites this paper as [34]
Data supporting specific dosages and intensities of progressive resistance training needed to enhance strength, power, muscle mass, bone density, and overall functional capacity is not yet fully defined.
“data supporting specific dosages and intensities of PRT needed to enhance strength, power, muscle mass, bone density, and overall functional capacity is not yet fully defined [4,5]”
From Global consensus on optimal exercise recommendations for enhancing healthy longevity in older adults (ICFSR) (2025) · cites this paper as [5]
Data supporting specific dosages and intensities of PRT needed to enhance strength, power, muscle mass, bone density, and overall functional capacity is not yet fully defined.
“Notably, data supporting specific dosages and intensities of PRT needed to enhance strength, power, muscle mass, bone density, and overall functional capacity is not yet fully defined [4,5].”
From Global consensus on optimal exercise recommendations for enhancing healthy longevity in older adults (ICFSR) (2025) · cites this paper as [5]
Type 2 diabetes is marked by accelerated cellular ageing, reflected in biochemical changes known as the hallmarks of ageing.
“T2DM is characterized by accelerated cellular ageing, as shown by an increase in biochemical changes that underlie the progressive loss of tissue integrity and function, collectively known as the hallmarks of ageing6.”
From Exercise activates AMPK in mouse and human pancreatic islets to decrease senescence (2024) · cites this paper as [6]
The specific molecular mechanisms underlying cellular aging and loss of organ function are still poorly understood.
“Yet, the specific molecular mechanisms underlying cellular aging and loss of organ function are still poorly understood (177).”
From Wound repair and regeneration: Mechanisms, signaling, and translation (2014) · cites this paper as [177]
Cellular senescence is a key component of human aging that can be induced by DNA damage, cellular stress, telomere shortening, and activation of oncogenes.
“Cellular senescence is a key component of human aging that can be induced by a range of stimuli, including DNA damage, cellular stress, telomere shortening, and the activation of oncogenes.”
From Senescence and Cancer: A Review of Clinical Implications of Senescence and Senotherapies (2020) · cites this paper as [8]
Aging is a risk factor for chronic diseases, atherosclerosis, cardiovascular diseases, stroke, kidney failure, chronic lung disease, cancers, diabetes, osteoporosis, arthritis, blindness, dementia, and neurodegenerative diseases.
“Aging is one of the risk factors for chronic diseases, atherosclerosis, cardiovascular diseases, stroke, kidney failure, chronic lung disease, cancers, diabetes, osteoporosis, arthritis, blindness, dementia, and neurodegenerative diseases [467,468].”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [468]
P53 can cause cellular senescence by regulating the cell cycle via inhibition of CDK4 and CDK6.
“P53 can cause cellular senescence [42] by regulating the cell cycle via inhibition of cyclin-dependent kinase (CDK) 4 and CDK6 [5, 43] (Fig. 2).”
From Immunosenescence: a key player in cancer development (2020) · cites this paper as [5]
Aging sensitivity of basic cellular pathways and cellular senescence contribute to declining adaptive immunity.
“Certainly, sensitivity of basic cellular pathways to aging and cellular senescence contribute”
From Successful and Maladaptive T Cell Aging (2017) · cites this paper as López-Otín et al., 2013
Activation of cellular senescence is considered one of the hallmarks of aging.
“the activation of cellular senescence is considered one of the hallmarks of aging”
From Integrin Beta 3 Regulates Cellular Senescence by Activating the TGF-β Pathway (2017) · cites this paper as López-Otín et al., 2013
Sterile inflammation and altered immune function are considered hallmarks of aging, sometimes called inflamm-aging.
“Altered immune function, including sterile inflammation, is considered a hallmark of the aging process, sometimes referred to as “inflamm-aging” (Franceschi et al., 2007; Lopez-Otin et al., 2013).”
From Cytoplasmic DNA: sources, sensing, and role in aging and disease (2021) · cites this paper as Lopez-Otin et al., 2013
The hallmarks of aging include stem cell exhaustion, altered intercellular communication, genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, altered nutrient and growth factor sensing, mitochondrial dysfunction and cellular senescence.
“These hallmarks of aging include stem cell exhaustion, altered intercellular communication, genomic instability and telomere attrition, epigenetic alterations, loss of protein homeostasis (proteostasis), altered nutrient and growth factor sensing, mitochondrial dysfunction and cellular senescence [3].”
From Aging of the immune system: Focus on inflammation and vaccination (2016) · cites this paper as [3]
A large body of experimental evidence across organisms from yeast to primates indicates at least nine evolutionarily conserved hallmarks of aging that derive from a small number of basic aging processes.
“a very large body of experimental evidence from a wide variety of organisms ranging from yeast to primates strongly suggests there are at least nine evolutionarily conserved hallmarks of aging that almost certainly derive from a small handful of basic aging processes [3].”
From Aging of the immune system: Focus on inflammation and vaccination (2016) · cites this paper as [3]
Hallmarks of aging are interconnected, and perturbation of one can affect others.
“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 López-Otín et al., 2013
Molecular and cellular decline of aging can be organized into evolutionarily conserved hallmarks.
“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 López-Otín et al., 2013
With age, telomere attrition occurs, somatic DNA mutations accumulate, transposons activate, and chromosomal abnormalities increase.
“With age, telomere attrition occurs, somatic DNA mutations accumulate, and transposons activate. There is also an increase in the rate of chromosomal abnormalities, some of which are oncogenic.”
From The Aging Epigenome (2016) · cites this paper as López-Otín et al., 2013
Increases in senescent cells and declines in tissue regeneration due to stem cell proliferation loss are hallmarks of aging.
“An increase in the number of senescent cells and a decline in tissue regeneration due to the loss of stem cell proliferation are both hallmarks of aging (López-Otín et al., 2013).”
From The Aging Epigenome (2016) · cites this paper as López-Otín et al., 2013
Changes in nutrient sensing and signaling are important hallmarks of aging.
“Changes in nutrient sensing and signaling are important hallmarks of aging (López-Otín et al., 2013).”
From The Aging Epigenome (2016) · cites this paper as López-Otín et al., 2013
Accumulation of DNA damage is a conserved hallmark of cancer and aging.
“The accumulation of DNA damage is a conserved hallmark of cancer and aging (1).”
From Controlled DNA double-strand break induction in mice reveals post-damage transcriptome stability (2016) · cites this paper as [1]
The absence of mtDNA histones and the lack of an efficient proofreading system are responsible for a progressive increase of somatic mtDNA mutations over the life course.
“The absence of mtDNA histones and the lack of an efficient proofreading system are thought to be responsible for a progressive increase of somatic mtDNA mutations over the life course [27].”
From Role of Age-Related Mitochondrial Dysfunction in Sarcopenia (2020) · cites this paper as [27]
Genomic instability caused by single- or double-strand breaks that activate the DNA damage response is an ageing hallmark and can originate from external or internal sources.
“Genomic instability induced by single-strand breaks or double-strand breaks triggering the DNA damage response (DDR) is a hallmark of ageing2, and can arise from both exogenous and endogenous sources79.”
From Mitochondrial and metabolic dysfunction in ageing and age-related diseases (2022) · cites this paper as [2]
Ageing is multifactorial involving genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intracellular communication.
“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 Lopez-Otin et al., 2013
Ageing-related failure of homeostasis mechanisms contributes to articular cartilage degeneration and osteoarthritis.
“Ageing-related failure of homeostasis mechanisms contributes to articular cartilage degeneration and osteoarthritis (OA)”
From Fibrates as drugs with senolytic and autophagic activity for osteoarthritis therapy (2019) · cites this paper as [1]
Epigenetic alteration is a hallmark of ageing.
“Epigenetic alteration is a hallmark of ageing4, and recent studies have demonstrated cellular and functional rejuvenation by transient epigenetic reprogramming17,51,52.”
From Measuring biological age using omics data (2022) · cites this paper as [4]
Biological ageing is enormously complex and is thought to be driven by the interaction of multiple dysregulated cellular and biochemical processes.
“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 [4]
Loss of proteostasis is a hallmark of ageing, and other hallmarks of ageing imply alterations in the proteome such as differential levels of insulin and peptide hormones, signalling proteins, and inflammatory cytokines.
“Additionally, loss of proteostasis is a hallmark of ageing4,100, and other hallmarks of ageing, such as dysregulated nutrient sensing, altered intercellular communication and cellular senescence, also imply alterations in the proteome such as differential levels of insulin and peptide hormones, signalling proteins, and inflammatory cytokines.”
From Measuring biological age using omics data (2022) · cites this paper as [4]
Much of the basic biology of ageing seems largely conserved among many species with very different lifespans.
“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 [4]
Aging has physiological effects on both the host and the microbiome, suggesting that host-microbiota interactions impact the progression and qualities of age-related changes.
“Aging has physiological effects on both the host (23) and the microbiome (24), suggesting that host–microbiota interactions impact the progression and qualities of age-related changes.”
From Senolytic Combination of Dasatinib and Quercetin Alleviates Intestinal Senescence and Inflammation and Modulates the Gut Microbiome in Aged Mice (2021) · cites this paper as [23]
Aging, the time-dependent functional decline of organs and tissues, is the biggest risk factor for many diseases, including several neurodegenerative and cardiovascular disorders.
“Aging, the time-dependent functional decline of organs and tissues, is the biggest risk factor for many diseases, including several neurodegenerative and cardiovascular disorders 1 .”
From Single-cell transcriptomic profiling of the aging mouse brain (2019) · cites this paper as [1]
While there may be hallmarks of aging that occur in most cell types, such as mitochondrial dysfunction and loss of proteostasis, the data argue against the hypothesis that aging induces a single universal molecular program in all cells and tissues.
“Thus, while there may be hallmarks of aging that occur in most cell types, such as mitochondrial dysfunction and loss of proteostasis 1,4,54 , our data argue against the hypothesis that aging induces a single universal molecular program in all cells and tissues 16 .”
From Single-cell transcriptomic profiling of the aging mouse brain (2019) · cites this paper as [1]
Of the only 7 down-regulated genes in the 82-gene set, protein homeostasis genes Dnajb1, Hsph1 and Ahsa1, as well as collagen synthesis gene P4ha1, were found, which is in line with perturbed protein quality control mechanisms as a hallmark of aging.
“Interestingly, of the only 7 down-regulated genes in this set, we found protein homeostasis genes Dnajb1 , Hsph1 and Ahsa1 , as well as collagen synthesis gene P4ha1 , which is in line with perturbed protein quality control mechanisms as a hallmark of aging (López-Otín et al., 2013) (Figure 2B).”
From Atlas of the aging mouse brain reveals white matter as vulnerable foci (2023) · cites this paper as López-Otín et al., 2013

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1 retracted

RETRACTED: Endurance exercise rescues progeroid aging and induces systemic mitochondrial rejuvenation in mtDNA mutator mice
Safdar, A., Bourgeois, J. M., Ogborn, D. I., Little, J. P., Hettinga, B. P., Akhtar, M., Thompson, J. E., Melov, S., Mocellin, N. J., Kujoth, G. C., et al. (2011) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1019581108 · Cited by 358 · see citing works
Retracted
Hallmarks of Cancer: The Next Generation
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Ageing and the pathogenesis of osteoarthritis
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Autophagy in malignant transformation and cancer progression
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Biomolecular condensates at the nexus of cellular stress, protein aggregation disease and ageing
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Spermidine in health and disease
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Antioxidant and Oxidative Stress: A Mutual Interplay in Age-Related Diseases
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Ageing, neurodegeneration and brain rejuvenation
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Somatic mutant clones colonize the human esophagus with age
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Mitochondrial generation of superoxide and hydrogen peroxide as the source of mitochondrial redox signaling
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ROS, Cell Senescence, and Novel Molecular Mechanisms in Aging and Age‐Related Diseases
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Authors: López-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G.
Affiliations: Max Planck Institute for Biology of Ageing (DE)
Spanish National Cancer Research Centre (ES)
Inserm (FR)
Corresponding author: Serrano, Manuel
ORCID: Serrano, Manuel
Kroemer, Guido
Venue: Cell
Publisher: Elsevier BV
Published: 2013-06
Volume: 153
Issue: 6
Pages: 1194-1217
ISSN: 0092-8674 (ISSN-L)
DOI: 10.1016/j.cell.2013.05.039
PMC: PMC3836174
OpenAlex: W2126525177
Cited by: 14,982
References: 305
Citations by year: 2026: 1358 · 2025: 1511 · 2024: 1522 · 2023: 1652 · 2022: 1695 · 2021: 1616 · 2020: 1376 · 2019: 1102 · 2018: 949 · 2017: 738 · 2016: 560 · 2015: 521 · 2014: 295 · 2013: 77 · 2012: 1
FWCI: 29.76
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 370 d)
Locations: Cell (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Consultation of the Doctoral Thesis Database (TESEO) (Ministerio de Educación, Cultura y Deporte) (submittedVersion, cc-by-nc-nd)
MPG.PuRe (Max Planck Society) (submittedVersion)
Funders: Wellcome Trust (098565)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Keywords: aging, hallmarks of aging, genomic instability, telomere shortening, epigenetic modifications, proteostasis, nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, intercellular communication, mammalian aging
MeSH terms: Aging, Animals, Humans, Telomere, Cellular Senescence, Genomic Instability, Epigenesis, Genetic

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