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When Poldip2 is deficient, it induces protein O-GlcNAcylation and inhibits the ubiquitin-proteasome system through metabolic reprogramming (TCA cycle inhibition, glycolytic activity, increased HBP activity), resulting in the accumulation of polyubiquitinated proteins in the nucleus to maintain the stability of SRF, ultimately leading to VSMC differentiation [136]

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However, clinical trials on people have not been published to confirm this effect

Subsequently, injury receptors release the neuropeptide calcitonin gene-related peptide (CGRP) into infected tissues, which inhibits neutrophil recruitment and the opsonophagocytic killing of S

Erastin, a ferroptosis-inducing agent, sensitized cancer cells to X-ray irradiation via glutathione starvation in vitro and in vivo