Mitophagy in neurodegeneration: crosstalk between PRKN/parkin-dependent and PRKN-independent pathways.
Level 5 - mechanism / opinion, no new human data
Narrative review of biological mechanisms without systematic search or original human data
PubMed 42533617 · doi:10.1080/15548627.2026.2711596
What was done
This narrative review synthesized literature on neuronal mitochondrial quality control, describing the canonical PINK1-PRKN/parkin-dependent mitophagy pathway alongside PRKN-independent mechanisms (ubiquitin-dependent, receptor-mediated, and lipid-mediated pathways) and their roles in neurodegenerative disease pathogenesis.
What was found
The abstract reports no numerical data or quantitative outcomes. It describes qualitative models showing that PRKN-dependent and PRKN-independent mitophagy pathways intersect and functionally compensate for one another, and that failure of these quality control networks promotes neurodegenerative onset and progression.
Why it matters
Clarifying the overlap and compensation between distinct mitophagy mechanisms identifies broader therapeutic targets for neurodegenerative disorders beyond single-pathway interventions.
Limits
The paper is a narrative review presenting no new experimental data, systematic search protocol, or meta-analysis. Findings are purely mechanistic, and clinical applicability or effect sizes in human populations are not reported.
Cited by
- supports Mitophagy is the cellular process of selectively degrading and recycling poorly functioning mitochondria.