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Chow E, Harris K, Fan G, Tsao M, Sze WM

10.1038/s41467-020-14993-8 35 GuillaudL.DimitrovD.TakahashiT

Complexes III, IV, and V are also have reported glutathionylation sites and glutathionylation inhibits ATP synthase, which has been related to oxidative-distress mediated heart disease [ 91 93 ]

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Similarly, a previous study has noted that IRAK4 inhibition (IRAK4i) mitigates RA joint inflammation by reprogramming metabolic dysfunction in synovial macrophages and FLSs (37)

Mitochondrial swelling, vesicle formation, and somatic cristae breakage were observed in the CuSO4-induced kidney injury model, nip3-like protein (NIX)/BNIP3 mRNA and protein levels were significantly upregulated, and the number of mitochondrial and lysosomal fluorescent aggregation sites was increased, suggesting that CuSO4 treatment promotes the onset of BNIP3/NIX-mediated mitophagy, and that co-treatment with CuSO4 and an inhibitor of mitophagy significantly exacerbates mitochondrial dysfunction ( In vivo experiments further confirmed that FLIPUS could alleviate ECM loss and chondrocyte apoptosis in a destabilization of the medial meniscus (DMM) mouse model through mitophagy mediated by FUNDC1, thereby exerting a protective effect on cartilage (Ye et al., 2023)