Abstract

Diabetes is one of the risk factors for disc degeneration, but the exact mechanism is still unclear. Misfolding and aggregation of human islet amyloid polypeptide (hIAPP) is an important factor in diabetes. hIAPP proteins misfold from monomers to β-sheet-rich oligomers, destroy the permeability of the cell membrane and cause abnormal cell function and death. Under the pathological state of diabetes, hIAPP oligomers can promote the expression and secretion of the inflammatory factor IL-1β, while IL-1β-mediated inflammatory response is the pathogenesis basis of intervertebral disc degeneration. Thus, amyloid hIAPP aggregation accelerates disc degeneration in the pathological state of diabetes.

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