Inflammatory Mediators of Endothelial Dysfunction.
Eirini DriEvangelos LampasGeorge LazarosEmilia LazarouPanagiotis TheofilisCostas TsioufisDimitris TousoulisPublished in: Life (Basel, Switzerland) (2023)
Endothelial dysfunction (ED) is characterized by imbalanced vasodilation and vasoconstriction, elevated reactive oxygen species (ROS), and inflammatory factors, as well as deficiency of nitric oxide (NO) bioavailability. It has been reported that the maintenance of endothelial cell integrity serves a significant role in human health and disease due to the involvement of the endothelium in several processes, such as regulation of vascular tone, regulation of hemostasis and thrombosis, cell adhesion, smooth muscle cell proliferation, and vascular inflammation. Inflammatory modulators/biomarkers, such as IL-1α, IL-1β, IL-6, IL-12, IL-15, IL-18, and tumor necrosis factor α, or alternative anti-inflammatory cytokine IL-10, and adhesion molecules (ICAM-1, VCAM-1), involved in atherosclerosis progression have been shown to predict cardiovascular diseases. Furthermore, several signaling pathways, such as NLRP3 inflammasome, that are associated with the inflammatory response and the disrupted H2S bioavailability are postulated to be new indicators for endothelial cell inflammation and its associated endothelial dysfunction. In this review, we summarize the knowledge of a plethora of reviews, research articles, and clinical trials concerning the key inflammatory modulators and signaling pathways in atherosclerosis due to endothelial dysfunction.
Keyphrases
- oxidative stress
- nitric oxide
- cardiovascular disease
- cell proliferation
- clinical trial
- reactive oxygen species
- inflammatory response
- smooth muscle
- human health
- signaling pathway
- endothelial cells
- cell adhesion
- healthcare
- small molecule
- emergency department
- randomized controlled trial
- escherichia coli
- dna damage
- rheumatoid arthritis
- coronary artery disease
- anti inflammatory
- systematic review
- epithelial mesenchymal transition
- toll like receptor
- cell death
- cystic fibrosis
- replacement therapy
- smoking cessation
- cardiovascular risk factors