Hallmarks of aging: An expanding universe.
Level 5 - mechanism / opinion, no new human data
Narrative review and conceptual framework without new empirical data or systematic review methodology.
PubMed 36599349 · doi:10.1016/j.cell.2022.11.001
What was done
The authors synthesized biogerontology literature into a conceptual framework based on three criteria: age-associated manifestation, experimental acceleration of aging when accentuated, and deceleration or reversal of aging upon therapeutic targeting.
What was found
The authors proposed twelve interconnected hallmarks of aging: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, disabled macroautophagy, deregulated nutrient-sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, altered intercellular communication, chronic inflammation, and dysbiosis. The abstract reports no empirical numbers or quantitative effect sizes.
Why it matters
This paper provides an updated, widely referenced taxonomy of the primary molecular and cellular processes proposed to drive organismal aging.
Limits
This is a narrative framework paper presenting expert categorization rather than an empirical trial or systematic review. No original human or animal data, sample sizes, or quantitative comparisons among the hallmarks are provided in the abstract.
Cited by
- context Mitochondrial dysfunction is the common root cause of major chronic diseases including cancer, type 2 diabetes, depression, and Alzheimer's disease.