Unveiling the new horizons of atherosclerosis: the crossroads of inflammation, pyroptosis, and immunity
TL;DR
This review provides a systematic overview of immune microenvironment remodeling and the mechanisms of pyroptosis during the onset and progression of atherosclerosis, and summarizes emerging therapeutic strategies targeting immune regulation and pyroptosis pathways, including NLRP3 inhibitors, cytokine- targeting agents, and nano-drug delivery systems.
Abstract
Atherosclerosis (AS) is a chronic cardiovascular disease. Traditional lipid-lowering treatments have not fully reduced the risk of disease onset in high-risk patients. This review provides a systematic overview of immune microenvironment remodeling and the mechanisms of pyroptosis during the onset and progression of atherosclerosis. Studies have shown that AS is not only related to abnormal lipid metabolism, but also closely associated with inflammatory responses, activation of immune cells, and programmed cell death. Immune cells, including macrophages, T cells, and B cells, play key roles in plaque formation, progression, and rupture. At the same time, NLR family pyrin domain containing 3 (NLRP3) inflammasome-mediated pyroptosis exacerbates plaque instability by promoting the release of inflammatory mediators, including Interleukin-1β (IL-1β) and interleukin-18 (IL-18), We further summarize emerging therapeutic strategies targeting immune regulation and pyroptosis pathways, including NLRP3 inhibitors, cytokine-targeted agents, and nano-drug delivery systems, thereby offering new perspectives for the precise treatment of AS.