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Atherosclerosis (AS) represents a chronic inflammatory disorder of the vascular system, characterized by complex interactions between immune cell surface markers and programmed cell death mechanisms. The Fas ligand (FasL), prominently expressed on immune cells, serves as a crucial mediator of apoptotic signaling pathways that significantly influence disease progression. Clinically, AS manifests through acute cardiovascular events triggered by the rupture of unstable plaques, subsequent platelet aggregation, and thrombus formation, ultimately causing vascular stenosis or complete occlusion.
At the pathological level, AS development involves focal lipid accumulation within arterial walls, accompanied by smooth muscle cell proliferation and extracellular matrix deposition, culminating in mature atherosclerotic plaque formation. The inflammatory cascade in AS engages multiple immune cell populations throughout all disease stages, from initial endothelial injury to advanced plaque destabilization. Of particular importance is the Fas/FasL system, which orchestrates programmed cell death through specific receptor-ligand interactions at immune cell surfaces.
While cell death constitutes a vital physiological process for tissue homeostasis, its dysregulation contributes significantly to AS pathogenesis. The Fas/FasL pathway represents a prototypical example of regulated cell death, distinct from passive necrosis resulting from acute cellular injury. This system not only mediates classical apoptosis but also interacts with alternative cell death modalities, including necroptosis, pyroptosis, and ferroptosis, which become activated under pathological conditions.
The intricate crosstalk between these cell death pathways, frequently modulated by FasL-expressing immune cells, profoundly impacts atherosclerotic lesion development through multiple mechanisms. Our research focuses on elucidating how FasL-mediated cell death pathways contribute to AS progression, with particular emphasis on their role in plaque stability, inflammatory responses, and vascular remodeling. These investigations aim to identify novel therapeutic targets within cell death regulatory networks for more effective AS management.