Pericytes are multifunctional mural cells essential for maintaining capillary integrity and regulating vascular tone. Under conditions of acute or chronic hyperglycemia, as observed in metabolic syndrome, pericytes show a profound molecular dysfunction. These include oxidative and nitrosative stress, mitochondrial fragmentation, impaired autophagy, and activation of pro-inflammatory transcription factors such as NF-κB. The resulting pericyte dropout contributes to microvascular instability, enhanced vascular permeability, and tissue hypoxia, particularly in vulnerable regions such as the retina, pancreas, and brain. Moreover, hyperglycemia-induced VEGF overexpression further exacerbates angiogenic imbalance and endothelial-pericyte uncoupling. This research synthesizes up-to-date evidence on pericyte vulnerability in metabolic syndrome, highlighting early biomarkers and potential therapeutic targets in preventing microvascular complications.
PAVLOVSCHI et al. (Wed,) studied this question.