Frontiers in Endocrinology · 5 authors, 5 centres
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This narrative review summarizes the bidirectional molecular interactions between the protein HMGB1 and autophagy in the context of diabetes and its complications. The central result is that HMGB1 can activate autophagy, while autophagy regulates HMGB1's secretion and degradation, creating a complex interplay that contributes to diabetic pathology.
This narrative review examines the molecular interplay between HMGB1 and autophagy in diabetes and its complications. It synthesizes preclinical and mechanistic evidence, showing that intracellular HMGB1 promotes autophagy by binding to Beclin1, while extracellular HMGB1 regulates autophagy via RAGE. Autophagy, in turn, controls HMGB1's nuclear-cytoplasmic translocation and secretion. In diabetes, this interplay is linked to insulin resistance via pathways like NF-κB and to organ damage (e.g., in cardiomyopathy, nephropathy). The review notes that the effects of autophagy can be protective or harmful depending on context and that the exact mechanisms require further study.
