TL;DR
It is highlighted that mitophagy mainly plays a protective role against liver fibrosis, whereas excessive mitophagy may exacerbate liver fibrosis by clearing healthy mitochondria aberrantly.
This review summarizes the principal epigenetic changes involved in HSC activation, initiation/progression of liver fibrosis, and discusses recent interventions designed to modulate these epigenetic changes.
The core mechanisms of how inter‐organelle network disruptions drive fibrosis are clarified, with the goal of identifying critical organelle nodes to disrupt pathogenic metabolic reprogramming and ultimately provide a rationale for developing new treatments.
Progressive hepatic fibrosis is the principal determinant of morbidity and mortality in metabolic dysfunction-associated steatotic liver disease and steatohepatitis (MASLD/MASH). Mitochondrial dysfunction is a hallmark of MASH, and the release of mitochondrial damage-associated molecular patterns (mito-DAMPs) from inju...
This review summarizes the molecular mechanisms underlying the crosstalk among mitophagy, pyroptosis, and macrophage polarization in CVD, with particular emphasis on myocardial infarction and myocardial ischemia-reperfusion injury.
The vital role of mitophagy in kidney diseases is examined, the potential of mitophagy-targeted therapies are discussed, and detailed alterations in specific mitophagy-related proteins associated with kidney diseases are described.
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