Biology of Aging & Longevity

Hallmarks of aging, senolytics, epigenetic clocks, partial reprogramming, mTOR and other geroprotective interventions.

305 papersnewest Nov 1, 2026

Most influential

  • Hallmarks of aging: An expanding universe
    Review6,534 citationsdoi:10.1016/j.cell.2022.11.001
  • The Hallmarks of Aging
    Review14,978 citationsdoi:10.1016/j.cell.2013.05.039
  • DNA methylation age of human tissues and cell types

    Background It is not yet known whether DNA methylation levels can be used to accurately predict age across a broad spectrum of human tissues and cell types, nor whether the resulting age prediction is a biologically meaningful measure. Results I developed a multi-tissue predictor of age that allows one to estimate the DNA methylation age of most tissues and …

    Abstract excerpt by Horvath S, CC-BY, https://doi.org/10.1186/gb-2013-14-10-r115; truncated.

    Article5,694 citationsdoi:10.1186/gb-2013-14-10-r115
  • Hallmarks of Cellular Senescence
    Review2,597 citationsdoi:10.1016/j.tcb.2018.02.001
  • SARS-CoV-2 is associated with changes in brain structure in UK Biobank

    . However, it remains unknown whether the impact of SARS-CoV-2 infection can be detected in milder cases, and whether this can reveal possible mechanisms contributing to brain pathology. Here we investigated brain changes in 785 participants of UK Biobank (aged 51-81 years) who were imaged twice using magnetic resonance imaging, including 401 cases who teste…

    Abstract excerpt by Gwenaëlle Douaud et al., CC-BY, https://doi.org/10.1038/s41586-022-04569-5; truncated.

    Article1,645 citationsdoi:10.1038/s41586-022-04569-5
  • The Achilles' heel of senescent cells: from transcriptome to senolytic drugs

    The healthspan of mice is enhanced by killing senescent cells using a transgenic suicide gene. Achieving the same using small molecules would have a tremendous impact on quality of life and the burden of age-related chronic diseases. Here, we describe the rationale for identification and validation of a new class of drugs termed senolytics, which selectively…

    Abstract excerpt by Zhu Y et al., CC-BY, https://doi.org/10.1111/acel.12344; truncated.

    Article2,112 citationsdoi:10.1111/acel.12344
  • A new gene set identifies senescent cells and predicts senescence-associated pathways across tissues

    Although cellular senescence drives multiple age-related co-morbidities through the senescence-associated secretory phenotype, in vivo senescent cell identification remains challenging. Here, we generate a gene set (SenMayo) and validate its enrichment in bone biopsies from two aged human cohorts. We further demonstrate reductions in SenMayo in bone followin…

    Abstract excerpt by Saul D et al., CC-BY, https://doi.org/10.1038/s41467-022-32552-1; truncated.

    Article1,042 citationsdoi:10.1038/s41467-022-32552-1
  • Cellular senescence mediates fibrotic pulmonary disease

    Idiopathic pulmonary fibrosis (IPF) is a fatal disease characterized by interstitial remodelling, leading to compromised lung function. Cellular senescence markers are detectable within IPF lung tissue and senescent cell deletion rejuvenates pulmonary health in aged mice. Whether and how senescent cells regulate IPF or if their removal may be an efficacious …

    Abstract excerpt by Schafer MJ et al., CC-BY, https://doi.org/10.1038/ncomms14532; truncated.

    Article1,435 citationsdoi:10.1038/ncomms14532
  • Mitochondrial dysfunction in cell senescence and aging

    Mitochondrial dysfunction and cell senescence are hallmarks of aging and are closely interconnected. Mitochondrial dysfunction, operationally defined as a decreased respiratory capacity per mitochondrion together with a decreased mitochondrial membrane potential, typically accompanied by increased production of oxygen free radicals, is a cause and a conseque…

    Abstract excerpt by Satomi Miwa et al., CC-BY, https://doi.org/10.1172/jci158447; truncated.

    Review1,060 citationsdoi:10.1172/jci158447
  • Senolytics decrease senescent cells in humans: Preliminary report from a clinical trial of Dasatinib plus Quercetin in individuals with diabetic kidney disease

    Background Senescent cells, which can release factors that cause inflammation and dysfunction, the senescence-associated secretory phenotype (SASP), accumulate with ageing and at etiological sites in multiple chronic diseases. Senolytics, including the combination of Dasatinib and Quercetin (D + Q), selectively eliminate senescent cells by transiently disabl…

    Abstract excerpt by Hickson LJ et al., CC-BY, https://doi.org/10.1016/j.ebiom.2019.08.069; truncated.

    Article1,119 citationsdoi:10.1016/j.ebiom.2019.08.069
  • Autophagy in healthy aging and disease
    Review1,313 citationsdoi:10.1038/s43587-021-00098-4
  • International Exercise Recommendations in Older Adults (ICFSR): Expert Consensus Guidelines

    The human ageing process is universal, ubiquitous and inevitable. Every physiological function is being continuously diminished. There is a range between two distinct phenotypes of ageing, shaped by patterns of living - experiences and behaviours, and in particular by the presence or absence of physical activity (PA) and structured exercise (i.e., a sedentar…

    Abstract excerpt by Míkel Izquierdo et al., CC-BY, https://doi.org/10.1007/s12603-021-1665-8; truncated.

    Article1,245 citationsdoi:10.1007/s12603-021-1665-8
  • Senolytics in idiopathic pulmonary fibrosis: Results from a first-in-human, open-label, pilot study

    Background Cellular senescence is a key mechanism that drives age-related diseases, but has yet to be targeted therapeutically in humans. Idiopathic pulmonary fibrosis (IPF) is a progressive, fatal cellular senescence-associated disease. Selectively ablating senescent cells using dasatinib plus quercetin (DQ) alleviates IPF-related dysfunction in bleomycin-a…

    Abstract excerpt by Justice JN et al., CC-BY, https://doi.org/10.1016/j.ebiom.2018.12.052; truncated.

    Article1,030 citationsdoi:10.1016/j.ebiom.2018.12.052
  • Declining NAD+ Induces a Pseudohypoxic State Disrupting Nuclear-Mitochondrial Communication during Aging
    Article1,478 citationsdoi:10.1016/j.cell.2013.11.037
  • Cellular senescence: the good, the bad and the unknown
    Review1,147 citationsdoi:10.1038/s41581-022-00601-z

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