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Oxidative Stress-Mediated Programmed Cell Death: a Potential Therapy Target for Atherosclerosis
Yuwu Chen1,2, Xing Luo1,2, Biyi Xu1,2
1Department of Cardiology, 2nd Affiliated Hospital of Harbin Medical University, Harbin, 150001, People's Republic of China.
Abstract:
Nowadays, as a type of orderly and active death determined by genes, programmed cell death (PCD), including apoptosis, pyroptosis, ferroptosis, and necroptosis, has attracted much attention owing to its participation in numerous chronic cardiovascular diseases, especially atherosclerosis (AS), a canonical chronic inflammatory disease featured by lipid metabolism disturbance. Abundant researches have reported that PCD under distinct internal conditions fulfills different roles of atherosclerotic pathological processes, including lipid core expansion, leukocyte adhesion, and infiltration. Noteworthy, emerging evidence recently has also suggested that oxidative stress (OS), an imbalance of antioxidants and oxygen free radicals, has the potential to mediate PCD occurrence via multiple ways, including oxidization and deubiquitination. Interestingly, more recently, several studies have proposed that the mediating mechanisms could effect on the atherosclerotic initiation and progression significantly from variable aspects, so it is of great clinical importance to clarify how OS-mediated PCD and AS interact. Herein, with the aim of summarizing potential and sufficient atherosclerotic therapy targets, we seek to provide extensive analysis of the specific regulatory mechanisms of PCD mediated by OS and their multifaceted effects on the entire pathological atherosclerotic progression.
Insights
Programmed cell death (PCD) plays a role in atherosclerosis (AS). Oxidative stress (OS) mediates PCD, influencing AS progression and offering potential therapeutic targets.
Area of Science:
- Cardiovascular Biology
- Cellular Pathology
- Molecular Medicine
Background:
- Programmed cell death (PCD), encompassing apoptosis, pyroptosis, ferroptosis, and necroptosis, is genetically regulated and implicated in chronic cardiovascular diseases.
- Atherosclerosis (AS), a chronic inflammatory condition marked by lipid metabolism disruption, involves various PCD types in its pathological processes like lipid core expansion and leukocyte infiltration.
- Oxidative stress (OS), an imbalance between free radicals and antioxidants, is increasingly recognized for its role in mediating PCD through mechanisms such as oxidation and deubiquitination.
Purpose of the Study:
- To analyze the specific regulatory mechanisms of PCD mediated by OS.
- To elucidate the multifaceted effects of OS-mediated PCD on the entire pathological progression of AS.
- To identify potential therapeutic targets for AS by understanding the interplay between OS and PCD.
Main Methods:
- Literature review and analysis of existing research on PCD, OS, and AS.
- Examination of molecular mechanisms linking OS to different PCD pathways.
- Synthesis of evidence on how OS-mediated PCD influences AS initiation and advancement.
Main Results:
- PCD, influenced by OS, contributes significantly to various stages of AS pathogenesis.
- OS modulates PCD through distinct molecular pathways, impacting cellular events in AS.
- The interaction between OS and PCD presents multifaceted effects on AS development.
Conclusions:
- Clarifying the mechanisms of OS-mediated PCD is crucial for understanding AS.
- Targeting OS-mediated PCD pathways may offer novel therapeutic strategies for AS.
- Further research into these interactions can lead to effective treatments for cardiovascular diseases.
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