AI Article Synopsis
- Diabetic vasculopathy significantly impacts the health of individuals with diabetes, primarily due to issues like hyperglycemia leading to endothelial dysfunction and affecting vascular smooth muscle.
- Emerging research suggests that hyperglycemia may disrupt the function of L-type calcium channels (Ca1.2), which are crucial for vascular health.
- The chapter highlights current knowledge on how elevated glucose levels influence Ca1.2, outlining the mechanisms at play and pointing out areas that require further investigation for understanding its role in diabetic conditions.
Article Abstract
Diabetic vasculopathy is a significant cause of morbidity and mortality in the diabetic population. Hyperglycemia, one of the central metabolic abnormalities in diabetes, has been associated with vascular dysfunction due to endothelial cell damage. However, studies also point toward vascular smooth muscle as a locus for hyperglycemia-induced vascular dysfunction. Emerging evidence implicates hyperglycemia-induced regulation of vascular L-type Ca channels Ca1.2 as a potential mechanism for vascular dysfunction during diabetes. This chapter summarizes our current understanding of vascular Ca1.2 channels and their regulation during physiological and hyperglycemia/diabetes conditions. We will emphasize the role of Ca1.2 in vascular smooth muscle, the effects of elevated glucose on Ca1.2 function, and the mechanisms underlying its dysregulation in hyperglycemia and diabetes. We conclude by examining future directions and gaps in knowledge regarding Ca1.2 regulation in health and during diabetes.
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| http://dx.doi.org/10.1016/bs.ctm.2022.09.003 | DOI Listing |
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