Abstract
Endothelial dysfunction is the most common pathological feature of diabetes, hypertension and atherosclerosis. Endothelial dysfunction can occur not only in large conduit arteries such as aorta and renal artery, but also in microvascular circulation in the retina and kidney. Decreased production and secretion of endothelium-derived vasodilator factors (mainly nitric oxide) or increased synthesis and release of vasoconstrictor factors (such as angiotensin II, endothelin-1, reactive oxygen species and cyclooxygenase metabolites) are the main causes of endothelial dysfunction, which is closely associated with pathogenesis of hypertension, diabetes, atherosclerosis, myocardial ischemia, and heart failure. This review briefly summarizes the mechanisms underlying endothelial dysfunction in relation to activation of the renin angiotensin system, cyclooxygenase 2, and bone morphogenetic protein 4, as well as increased oxidative stress and inflammatory response in blood vessels, hoping to identify the key molecular mediators of endothelial dysfunction, thereby providing new clues for both basic and translational research in cardio-metabolic biology and medicine.
| Translated title of the contribution | The pathogenesis of endothelial dysfunction |
|---|---|
| Original language | Chinese (Simplified) |
| Pages (from-to) | 691-698 |
| Journal | 中国科学:生命科学 |
| Volume | 52 |
| Issue number | 5 |
| Online published | 14 Mar 2022 |
| DOIs | |
| Publication status | Published - 2022 |
Research Keywords
- 内皮细胞功能障碍
- 肾素-血管紧张素系统
- 环氧合酶-2
- 骨形态发生蛋白 4
- 炎症反应
- 血流剪切力
- endothelial dysfunction
- renin-angiotensin-system
- cyclooxygenase-2
- bone morphogenetic protein 4
- inflammation
- shear stress
Fingerprint
Dive into the research topics of 'The pathogenesis of endothelial dysfunction'. Together they form a unique fingerprint.Projects
- 1 Finished
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GRF: Scavenging Mitochondrial ROS by UCP2 Attenuates Atherosclerosis through Suppression of Endoplasmic Reticulum Stress
HUANG, Y. (Principal Investigator / Project Coordinator)
1/01/20 → 5/12/23
Project: Research
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