ArticleAging cell2021
Senescent cells and the incidence of age-related diseases.
Article in Aging cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.
- Broad repression of DNA repair genes in senescent cells identified by integration of transcriptomic data.Nucleic acids research · 2025Pooled it
- Association of Molecular Senescence Markers in Late-Life Depression With Clinical Characteristics and Treatment Outcome.JAMA network open · 2022Trial
- A Deep-Learning Based Biomarker of Systemic Cellular Senescence Burden to Predict Mortality and Health Outcomes.Aging cell · 2026Article
- Restoration of circadian rhythm as novel targets against sarcopenia.Chinese medical journal · 2026Review
- Two modes of aging to explain why lifespans differ across species.Nature aging · 2026Article
- Article
- Dynamics of the end-of-life phase explained by the saturating removal model.bioRxiv : the preprint server for biology · 2026Article
- Metabolic reprogramming in diabetes and other endocrine and metabolic disorders: exploring the Warburg effect, ketones, and SGLT2 inhibitors.Reviews in endocrine & metabolic disorders · 2026Review
- Article
- Chronic inflammation as a driving factor for sarcopenia: an update on pathophysiology and future therapeutic targets.Frontiers in pharmacology · 2026Review
- The multistep pathogenic hypothesis of amyotrophic lateral sclerosis is incompatible with the epidemiological data.European journal of epidemiology · 2026Article
- TNFSF13 Drives Atherosclerosis Progression by Targeting Macrophage Senescence.International journal of medical sciences · 2026Article
- Pharmacological clearance of senescent cells reduces inflammation, endothelial damage and cardiac fibrosis in HFpEF.Cardiovascular research · 2025Article
- Global disease burden of interstitial lung disease and pulmonary sarcoidosis, 1990-2021, and forecast analysis over the next decade.Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2025Article
- Neurotoxicants driving glial aging: role of astrocytic aging in non-cell autonomous neurodegeneration.Toxicological sciences : an official journal of the Society of Toxicology · 2025Review
- Targeting Ferroptosis to Eliminate Senescent Cells: Mechanisms and Therapeutic Potential.Aging and disease · 2025Review
- Compression of morbidity by interventions that steepen the survival curve.Nature communications · 2025Article
- Natural polyphenols as novel interventions for aging and age-related diseases: Exploring efficacy, mechanisms of action and implications for future research.Chinese herbal medicines · 2025Review
- Metabolic Rewiring and Post-Translational Modifications: Unlocking the Mechanisms of Bone Turnover in Osteoporosis.Aging and disease · 2025Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Age-related diseases such as cancer, cardiovascular disease, kidney failure, and osteoarthritis have universal features: Their incidence rises exponentially with age with a slope of 6-8% per year and decreases at very old ages. There is no conceptual model which explains these features in so many diverse diseases in terms of a single shared biological factor. Here, we develop such a model, and test it using a nationwide medical record dataset on the incidence of nearly 1000 diseases over 50 million life-years, which we provide as a resource. The model explains incidence using the accumulation of senescent cells, damaged cells that cause inflammation and reduce regeneration, whose level rise stochastically with age. The exponential rise and late drop in incidence are captured by two parameters for each disease: the susceptible fraction of the population and the threshold concentration of senescent cells that causes disease onset. We propose a physiological mechanism for the threshold concentration for several disease classes, including an etiology for diseases of unknown origin such as idiopathic pulmonary fibrosis and osteoarthritis. The model can be used to design optimal treatments that remove senescent cells, suggeting that treatment starting at old age can sharply reduce the incidence of all age-related diseases, and thus increase the healthspan.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.