Arterial smooth muscle cells dysfunction in hyperglycaemia and hyperglycaemia associated with hyperlipidaemia: from causes to effects

Abstract

Given the important role of smooth muscle cells in arterial wall dysfunction in diabetes, as well as in diabetes associated with accelerated atherosclerosis, we provide a brief review of the recent achievements in identification of signalling molecules underlying their altered cellular responses, and examine the consequences of these pathological insults on smooth muscle cells properties. The original results emerging from the Golden Syrian hamster model (rendered diabetic or simultaneously hyperlipidaemic-diabetic) and from human aortic smooth muscle cells cultured in 25 mM glucose (to mimic diabetic condition) or sera of obese type 2 diabetic patients (to mimic the metabolic syndrome condition) are presented in this context. We conclude this review with several open issues disclosed by the most recent literature that deserve essential attention for targeting the translational medicine.

Regulation of Large Conductance Ca2+-activated K+ (BK) Channel β1 Subunit Expression by Muscle RING Finger Protein 1 in Diabetic Vessels

“…The mechanisms that underlie diabetic vascular disorders are multifactorial. Besides endothelium dysfunction, abnormal smooth muscle function also critically contributes to vascular pathology in diabetes, especially under the long-term conditions of glucotoxicity and lipotoxicity (49). A major cause of diabetic BK channel abnormality is attributed to the downregulation of BK-␤1 expression in vascular SMCs (26, 27), resulting in impaired BK channel sensitivity to Ca 2ϩ and voltage activation (26, 27).…”

Carpinus turczaninowii Extract May Alleviate High Glucose-Induced Arterial Damage and Inflammation

“…Increased proliferation and migration of VSMCs aggravates the progression of atherosclerosis by converting a fatty streak to an irreversible blood plaque [11]. Several studies have demonstrated that the vascular complications caused by hyperglycemia results from abnormal proliferation and migration of VSMCs [32,33,34] causing DM induced atherosclerosis [34].…”