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Inhibition of high mobility group box 1 (HMGB1) attenuates podocyte apoptosis and epithelial‐mesenchymal transition by regulating autophagy flux

Podocyte injury, characterized by podocyte hypertrophy, apoptosis, and epithelial‐mesenchymal transition (EMT), is the major causative factor of diabetic nephropathy (DN). Autophagy dysfunction is regarded as the major risk factor for podocyte injury including EMT and apoptosis. High mobility group box 1 (HMGB1) is involved in the progression of DN through the induction of autophagy. However, the underlying mechanism remains unknown.