Impairment in the function of insulin-producing pancreatic β-cells is a hallmark of both type 1 and 2 diabetes (T1D/T2D). Despite over a century of effort, there is still no precise treatment regimen available for acute diabetes. Enhancing the endogenous β-cells either by protecting them from apoptosis or dedifferentiation is a classic alternative to retaining the β-cell pool.
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