Protein kinase C: A potential therapeutic target for endothelial dysfunction in diabetes

• Published in: Journal of diabetes and its complications Vol. 37; no. 9; p. 108565
• Main Authors: Xiao, Qian, Wang, Dan, Li, Danyang, Huang, Jing, Ma, Feifei, Zhang, Haocheng, Sheng, Yingda, Zhang, Caimei, Ha, Xiaoqin
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.09.2023; Elsevier Limited
• Subjects: Alzheimer's disease; Apoptosis; Cardiac function; Cardiomyocytes; Cytokines; Diabetes; Diabetes mellitus; Endothelial cell; Inflammation; Ischemia; Kinases; Lymphocytes; Oxidative stress; Phosphorylation; Physiology; Protein kinase C; Proteins; Regulation; Smooth muscle; T cell receptors; Tumor necrosis factor-TNF; Oxidative stress; Protein kinase C; Endothelial cell; Inflammation; Diabetes mellitus
• ISSN: 1056-8727; 1873-460X
• DOI: 10.1016/j.jdiacomp.2023.108565

Protein kinase C (PKC) is a family of serine/threonine protein kinases that play an important role in many organs and systems and whose activation contributes significantly to endothelial dysfunction in diabetes. The increase in diacylglycerol (DAG) under high glucose conditions mediates PKC activation and synthesis, which stimulates oxidative stress and inflammation, resulting in impaired endothelial cell function. This article reviews the contribution of PKC to the development of diabetes-related endothelial dysfunction and summarizes the drugs that inhibit PKC activation, with the aim of exploring therapeutic modalities that may alleviate endothelial dysfunction in diabetic patients. •We summarize the role of PKC in the cardiovascular, nervous and immune systems.•We outline the mechanisms by which PKC leads to endothelial dysfunction in diabetes through activation of oxidative stress.•We summarise the mechanisms by which PKC induces endothelial dysfunction in diabetes through activation of inflammation.•We summarize the current drugs that can improve endothelial function by inhibiting PKC.