Skin Aging and Mitochondrial Dysfunction: Structural Changes, Mechanistic Insights, and Therapeutic Perspectives.
Level 5 - mechanism / opinion, no new human data
Narrative review of mechanistic literature and early-stage studies
PubMed 42133650 · doi:10.1155/omcl/5140711
What was done
This narrative review analyzed 49 scientific articles published between 2015 and 2025 retrieved from PubMed, Scopus, and ScienceDirect. The authors synthesized mechanistic insights and evaluated emerging therapeutic interventions targeting mitochondrial dysfunction in skin aging, including NAD+ precursors, coenzyme Q10, senolytics, and mitochondrial quality control modulators.
What was found
The abstract reports no numerical effect sizes or quantitative outcome statistics. It reports that advancing age correlates with declines in mitochondrial DNA copy number and increased reactive oxygen species production, contributing to cellular senescence, inflammaging, and the senescence-associated secretory phenotype. Preclinical and early clinical studies of mitochondrial-targeted therapies show promising effects on skin aging parameters, though based on small trials with short follow-up.
Why it matters
The paper synthesizes how mitochondrial genome instability and oxidative stress drive cutaneous senescence, framing mitochondrial pathways as plausible therapeutic targets for skin aging.
Limits
As a narrative review, it lacks a systematic review methodology or meta-analytic pooling. Included human evidence is constrained by small sample sizes, brief follow-up periods, limited longitudinal safety data, and a lack of standardized clinical biomarkers.
Cited by
- supports Mitochondria are the primary generator of reactive oxygen species in cells.