Juanjuan Chen1, Wanyu Tan2. 1. Jiangxi Province Key Laboratory of Laboratory Medicine, Department of Clinical Laboratory, The Second Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi, PR China. Electronic address: ndefy11330@ncu.edu.cn. 2. School of Public Health, Nanchang University, Nanchang 330006, Jiangxi, PR China.
Abstract
BACKGROUND: Diabetes can lead to serious pathological changes in the microvascular system, which in turn leads to functional damage of related tissues that affects the quality of life of patients. The mechanism of microcirculation disturbance in diabetes is not well understood; however, the inflammatory damage and dysgenesis of blood vessels based on oxidative and hyperosmotic stress is considered to be a key factor. In addition, with in-depth studies of platelet function, the study of platelet inflammatory function has become popular in recent years. OBJECTIVE: The present manuscript reviews the new knowledge of platelet immune inflammatory function and the mechanism of diabetic microangiopathy, and emphasizes the relationship between them. CONCLUSION: The nuclear factor-κB (NF-κB) pathway has always been regarded as a typical pro-inflammatory signaling pathway in different nucleated cells, and NF-κB is also expressed in platelets. Although the signaling pathway of NF-κB in platelets is not completely understood, numerous studies have confirmed its function in platelet immune inflammation. The signaling pathway of the development of diabetic microangiopathy is partially cross-linked with the platelet NF-κB pathway. In addition, platelets can release various chemokines to aggravate vascular endothelial cell injury, indicating that platelets may serve a key role in the mechanism of diabetic microangiopathy.
BACKGROUND:Diabetes can lead to serious pathological changes in the microvascular system, which in turn leads to functional damage of related tissues that affects the quality of life of patients. The mechanism of microcirculation disturbance in diabetes is not well understood; however, the inflammatory damage and dysgenesis of blood vessels based on oxidative and hyperosmotic stress is considered to be a key factor. In addition, with in-depth studies of platelet function, the study of platelet inflammatory function has become popular in recent years. OBJECTIVE: The present manuscript reviews the new knowledge of platelet immune inflammatory function and the mechanism of diabetic microangiopathy, and emphasizes the relationship between them. CONCLUSION: The nuclear factor-κB (NF-κB) pathway has always been regarded as a typical pro-inflammatory signaling pathway in different nucleated cells, and NF-κB is also expressed in platelets. Although the signaling pathway of NF-κB in platelets is not completely understood, numerous studies have confirmed its function in platelet immune inflammation. The signaling pathway of the development of diabetic microangiopathy is partially cross-linked with the platelet NF-κB pathway. In addition, platelets can release various chemokines to aggravate vascular endothelial cell injury, indicating that platelets may serve a key role in the mechanism of diabetic microangiopathy.