IHG-1 Increases Mitochondrial Fusion and Bioenergetic Function

摘要: Induced in high glucose-1 (IHG-1) is a conserved mitochondrial protein associated with diabetic nephropathy (DN) that amplifies profibrotic transforming growth factor (TGF)-β1 signaling and increases biogenesis. Here we report inhibition of endogenous IHG-1 expression results reduced respiratory capacity, ATP production, fusion. Conversely, overexpression leads to increased fusion also protects cells from reactive oxygen species-induced apoptosis. forms complexes known mediators fusion-mitofusins (Mfns) 1 2-and enhances the GTP-binding capacity Mfn2, suggesting acts as guanine nucleotide exchange factor. must be localized mitochondria interact Mfn1 this interaction necessary for IHG-1-mediated Together, these findings indicate novel regulator both dynamics bioenergetic function contributes cell survival following oxidant stress. We propose kidney disease viability actions TGF-β, leading renal proximal tubule dedifferentiation, an important event pathogenesis devastating condition.