Mitophagy in health and disease. Molecular mechanisms, regulatory pathways, and therapeutic implications.
Level 5 - mechanism / opinion, no new human data
Narrative review summarizing molecular mechanisms and therapeutic implications without systematic methodology or primary human data
PubMed 38758472 · doi:10.1007/s10495-024-01977-y
What was done
This narrative review synthesized the molecular mechanisms and regulatory networks governing mitophagy, focusing on PINK1/Parkin-mediated and receptor-mediated pathways (including BNIP3/NIX, FUNDC1, and Bcl2-L-13). It detailed post-translational modifications, signaling pathways, the decline in mitophagy efficiency during aging, and the role of mitophagy in conditions such as cancer, myocardial ischemia-reperfusion injury, Parkinson's disease, and Alzheimer's disease. It also surveyed potential therapeutic approaches, including dietary interventions, small molecules, drugs, and gene therapy.
What was found
The abstract provides a descriptive overview of pathways and disease associations but reports no specific quantitative data, sample sizes, or numerical effect estimates.
Why it matters
The paper synthesizes diverse mechanistic pathways linking mitochondrial quality control failure to age-related and degenerative pathologies, highlighting potential targets for future pharmacological and lifestyle interventions.
Limits
The review provides no primary empirical data and lacks a systematic search methodology or meta-analytic evaluation. The therapeutic feasibility and clinical translational efficacy of the discussed interventions are not quantified in the abstract.
Cited by
- supports The PINK/Parkin pathway marks damaged mitochondria for destruction, and inhibiting this pathway leads to the accumulation of dysfunctional mitochondria, reactive oxygen species production, and apoptotic trigger potential.