AI Networking Cookbook: Practical recipes for AI-assisted network automation and development
TL;DR
Current understanding of PINK1-Parkin-dependent and independent mitophagy pathways are summarized, highlighting mechanistic distinctions and coordinated regulation, as well as the expanding therapeutic potential of targeting mitophagy in disease.
This review provides a comprehensive overview of the best-characterized PINK1-PRKN/parkin-dependent mitophagy pathway and the expanding repertoire of PRKN-independent mechanisms, including additional ubiquitin-dependent, receptor-mediated, and lipid-mediated pathways.
Ten key PTMs, including lactylation, succinylation, succinylation, SUMOylation, and S-nitrosylation, acting on core regulators such as dynamin-related protein 1(DRP1), optic atrophy 1 (OPA1), Parkin, and mitochondrial Rho GTPase 1 (MIRO1) are summarized to provide a comprehensive resource for understanding mitochondria...
Mitophagy is increasingly recognized as a context-dependent regulator of cardiac metabolic adaptation rather than solely as a disposal pathway for damaged mitochondria. By coupling mitochondrial turnover to substrate selection, redox control, and inflammatory signaling, mitophagy can influence fatty acid oxidation (FAO...
Certain forms of mitochondrial impairment confer longevity, while disease-associated mitochondrial dysfunction triggers pathogenesis. The adaptive pathways that distinguish benefit from pathology remain unclear. Here we reveal that longevity induced by mitochondrial Complex I/nuo-6 mutation in C. elegans is dependent o...
It is hypothesized that FCCP-induced mitochondrial depolarization activates the PINK1-Parkin-mediated mitophagy pathway, culminating in the clearance of damaged mitochondria, and these findings demonstrate that FCCP robustly activates the canonical PINK1-Parkin mitophagy pathway in hASM cells.
Although mtISR has been characterized in primary mitochondrial myopathies, secondary mitochondrial dysfunction in neuromuscular disorders suggests that mtISR-related pathways may also be activated in these conditions, and its roles in skeletal muscle pathology are discussed.
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