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Necroptosis in atherosclerosis
Xiaofan Zhang1, Zhong Ren1, Wenxin Xu1
1Institute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan Province, International Joint Laboratory for Arteriosclerotic Disease Research of Hunan Province, Hengyang Medical School, University of South China, Hengyang 421001, China.
Insights
Necroptosis, a programmed cell death, contributes to atherosclerosis by promoting inflammation in vascular cells and macrophages within plaques. Understanding this process is key to developing new treatments for this leading cause of death.
Area of Science:
- Cardiovascular Biology
- Cellular Pathology
- Inflammatory Diseases
Background:
- Atherosclerosis is a major global cause of mortality, characterized by chronic inflammation.
- Key cellular players in atherosclerotic plaque development include vascular endothelial cells (VECs), vascular smooth muscle cells (VSMCs), and macrophages.
- Necroptosis, a form of programmed necrosis, is observed in advanced atherosclerotic lesions.
Purpose of the Study:
- To review the pathophysiological role of necroptosis in atherosclerosis.
- To explore the involvement of necroptosis in VECs, VSMCs, and macrophages within atherosclerotic plaques.
- To connect necroptosis mechanisms to the progression of atherosclerosis.
Main Methods:
- Literature review focusing on necroptosis and atherosclerosis.
- Analysis of studies investigating necroptosis in VECs, VSMCs, and macrophages.
- Synthesis of current understanding of necroptosis's impact on plaque development and inflammation.
Main Results:
- Necroptosis occurs in advanced atherosclerotic plaques.
- This programmed cell death influences the function of VECs, VSMCs, and macrophages.
- Necroptosis can promote a pro-inflammatory state, potentially accelerating atherosclerosis.
Conclusions:
- Necroptosis plays a significant pathophysiological role in atherosclerosis.
- Targeting necroptosis in VECs, VSMCs, and macrophages may offer therapeutic strategies.
- Further research is warranted to fully elucidate necroptosis's contribution to atherosclerosis.
Abstract:
Atherosclerosis, a chronic inflammatory disease, is a leading cause of death worldwide. Vascular endothelial cells (VECs), vascular smooth muscle cells (VSMCs) and macrophages play extremely vital roles in the formation of atherosclerotic plaques and subsequent atherosclerosis. Necroptosis, a caspase-independent programmed cell necrosis, occurs in advanced atherosclerotic plaques and has been implicated in VEC, VSMC and macrophage function. Although necroptosis may have considered as a defensive line against intracellular infection, it can induce a pro-inflammatory state, which will accelerate the disease process. Accordingly, necroptosis plays an important pathophysiologic role. In this review, we explore the role of necroptosis in VECs, VSMCs and macrophages in atherosclerotic plaques and their connection to atherosclerosis.
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