ReviewNature genetics2024
Distinguishing between driver and passenger mechanisms of aging.
Review in Nature genetics, 2024. 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.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Exploring accelerated aging as a target of bipolar disorder treatment: A systematic review.Journal of psychiatric research · 2024Pooled it
- Tissue-Level Transcriptomic Entropy Reveals Organ-Specific Aging Patterns and Predicts Cancer Progression.Aging cell · 2026Article
- Beyond sex determination: the Y chromosome in male cancers.Nature reviews. Cancer · 2026Review
- The OmniAge compendium of aging omic biomarkers links mitotic clocks to clonal hematopoiesis and causality.Nature communications · 2026Article
- A progeria syndrome links DNA hypermethylation to age-related pathology.Nature genetics · 2026Article
- Taking apart the DNA-methylation clock with an epigenetic progeria syndrome.Nature genetics · 2026Article
- Profiling the molecular and physiological effects of senolytic treatment on aged mice identifies immune, fibrotic and metabolic remodeling.Nature aging · 2026Article
- Open problems in ageing science: a roadmap for biogerontology.GeroScience · 2026Review
- Proteomic aging clocks in epidemiological studies: advances, applications and prospects.Nature aging · 2026Review
- Pleiotropy and disease interactors: the dual nature of genes linking ageing and ageing-related diseases.Biogerontology · 2026Article
- Molecular evolution of animal aging.The EMBO journal · 2026Review
- The purinergic receptor P2rx7 mediated ATP sensing is required to prevent bone aging by directing mitochondrial fitness of MSCs.Journal of advanced research · 2026Article
- The success-failure inversion in modern medicine.Frontiers in public health · 2026Article
- Epigenetic program of ontogenesis and hyperfunction theory: reinterpreting the mechanisms of aging.Frontiers in aging · 2026Article
- Prediction and analysis of anti-aging peptides using data augmentation and machine learning algorithms.BMC biology · 2025Article
- Do we actually need aging clocks?npj aging · 2025Review
- A full life cycle biological clock based on routine clinical data and its impact in health and diseases.Nature medicine · 2025Article
- The evolution of cancer and ageing: a history of constraint.Nature reviews. Cancer · 2025Review
- Unraveling the meta-hallmarks between senescent and tumor cells: A new perspective for senolytic drug discovery.Acta pharmaceutica Sinica. B · 2025Review
- An integrated multi-omic natural history study of human development, sexual dimorphism, and the effects of trisomy 21.Nature communications · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
Abstract
Understanding why we age is a long-standing question, and many mechanistic theories of aging have been proposed. Owing to limitations in studying the aging process, including a lack of adequate quantitative measurements, its mechanistic basis remains a subject of debate. Here, I explore theories of aging from the perspective of causal relationships. Many aging-related changes have been observed and touted as drivers of aging, including molecular changes in the genome, telomeres, mitochondria, epigenome and proteins and cellular changes affecting stem cells, the immune system and senescent cell buildup. Determining which changes are drivers and not passengers of aging remains a challenge, however, and I discuss how animal models and human genetic studies have been used empirically to infer causality. Overall, our understanding of the drivers of human aging is still inadequate; yet with a global aging population, elucidating the causes of aging has the potential to revolutionize biomedical research.
Indexed as
Identifiers
38242993What OpenQuestion holds
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.