Endothelial Dysfunction in the Cardiovascular System and Cardiac Injury

Abstract

The endothelium, composed of a single layer of endothelial cells, maintains vascular homeostasis by regulating vascular tone, coagulation, inflammation, and permeability. Under physiological conditions, it releases mediators such as nitric oxide (NO) that promote vasodilation and prevent thrombosis. However, exposure to cardiovascular risk factors like oxidative stress, inflammation, hypertension, diabetes, and metabolic disturbances leads to endothelial dysfunction (ED). This state is characterized by reduced NO bioavailability, elevated reactive oxygen species (ROS), and pro-inflammatory signaling, resulting in vascular constriction, platelet aggregation, and endothelial activation. ED plays a pivotal role in the onset and progression of atherosclerosis, hypertension, myocardial infarction, and heart failure. Emerging mechanisms, including endothelial senescence and endothelial-to-mesenchymal transition, further aggravate vascular and cardiac damage. As a reversible and early marker of cardiovascular injury, ED provides opportunities for early diagnosis and therapeutic intervention through lifestyle modification, antioxidants, and pharmacological agents aimed at restoring endothelial integrity and function.

Cite as:

Rakesh Sharma. (2026). Endothelial Dysfunction in the Cardiovascular System and Cardiac Injury. Journal of Advances in Nanotechnology and Its Applications, 8(1), 9–30. https://doi.org/10.5281/zenodo.19086375