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Furthermore, even after decades of maintaining tight glycemic control, susceptibility to disease progression can persist following a period of poor glycemic control through a process termed "glycemic memory." In response to chronically elevated glucose levels, a number of studies have identified molecular targets of the glucose-mediated protein posttranslational modification by the addition of an O-linked N-acetylglucosamine to impair contractility, calcium sensitivity, and mitochondrial protein function

(78) previously established that heat shock protein beta-1 (HSPB1) is a negative regulator of ferroptosis in cancer cells

Grtner R, Gasnier BC, Dietrich JW, Krebs B, Angstwurm MW

The two approaches converge on a common endpoint, reducing the burden of cellular senescence, through complementary upstream mechanisms

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