Research Progress and Molecular Mechanisms of Endothelial Cells Inflammation in Vascular-Related Diseases

Abstract

Endothelial cells (ECs) are widely distributed inside the vascular network, forming a vital barrier between the bloodstream and the walls of blood vessels. These versatile cells serve myriad functions, including the regulation of vascular tension and the management of hemostasis and thrombosis. Inflammation constitutes a cascade of biological responses incited by biological, chemical, or physical stimuli. While inflammation is inherently a protective mechanism, dysregulated inflammation can precipitate a host of vascular pathologies. ECs play a critical role in the genesis and progression of vascular inflammation, which has been implicated in the etiology of numerous vascular disorders, such as atherosclerosis, cardiovascular diseases, respiratory diseases, diabetes mellitus, and sepsis. Upon activation, ECs secrete potent inflammatory mediators that elicit both innate and adaptive immune reactions, culminating in inflammation. To date, no comprehensive and nuanced account of the research progress concerning ECs and inflammation in vascular-related maladies exists. Consequently, this review endeavors to synthesize the contributions of ECs to inflammatory processes, delineate the molecular signaling pathways involved in regulation, and categorize and consolidate the various models and treatment strategies for vascular-related diseases. It is our aspiration that this review furnishes cogent experimental evidence supporting the established link between endothelial inflammation and vascular-related pathologies, offers a theoretical foundation for clinical investigations, and imparts valuable insights for the development of therapeutic agents targeting these diseases.

The Impact of 3-MA on Autophagy and Atherosclerosis via Wnt/β-catenin and AMPK/mTOR Pathways

“…3-MA inhibits endothelial cell repair and aggravates the development of AS. Furthermore, in an in vitro experimental HUVECs model, the cholinine-derived metabolite trimethylamine n-oxide (3-MA) induced oxidative stress and activated the ROS-TXNIP-NLRP3 in ammasome signaling pathway, leading to EC in ammation and endothelial dysfunction, thereby increasing the risk of AS [15]. However, these reports did not clarify the relationship between Wnt/β-catenin and AMPK/mTOR pathway, which is supplemented by this study.…”