The Potential Therapeutic Prospect of PANoptosis in Heart Failure

被引:1
作者
Jia, Yunfeng [1 ]
Liu, Yayi [1 ]
Zuo, Yiming [1 ]
Zhang, Junping [1 ]
Li, Yanyang [2 ,3 ]
Liu, Xuezheng [1 ]
Lv, Shichao [1 ]
机构
[1] Tianjin Univ Tradit Chinese Med, Natl Clin Res Ctr Chinese Med Acupuncture & Moxibu, Dept Geriatr, Teaching Hosp 1, Tianjin 300381, Peoples R China
[2] Tianjin Med Univ Canc Inst & Hosp, Dept Integrated Tradit & Western Med, Tianjin 300060, Peoples R China
[3] Tianjin Univ Tradit Chinese Med, Grad Sch, Tianjin 301617, Peoples R China
关键词
PANoptosis; pyroptosis; apoptosis; necroptosis; cell death; heart failure; CELL-DEATH; INFLAMMASOME ACTIVATION; NLRP3; INFLAMMASOME; MYOCARDIAL-INFARCTION; MITOCHONDRIAL-DNA; OXIDATIVE STRESS; MOLECULAR SWITCH; APOPTOSIS; NECROPTOSIS; ZBP1;
D O I
10.2147/JIR.S485901
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Heart failure (HF) represents a serious manifestation or advanced stage of various cardiac diseases. HF continues to impose a significant global disease burden, characterized by high rates of hospitalization and fatality. Furthermore, the pathogenesis and pathophysiological processes underlying HF remain incompletely understood, complicating its prevention and treatment strategies. One significant pathophysiological mechanism associated with HF is the systemic inflammatory response. PANoptosis, a novel mode of inflammatory cell death, has been extensively studied in the context of infectious diseases, neurodegenerative disorders, cancers, and other inflammatory conditions. Recent investigations have revealed that PANoptosis-related genes are markedly dysregulated in HF specimens. Consequently, the PANoptosis-mediated inflammatory response may represent a potential mechanism and therapeutic target for HF. This paper conducts a comprehensive analysis of the molecular pathways that drive PANoptosis. We discuss its role and potential therapeutic targets in HF, thereby providing valuable insights for clinical treatment and the development of novel therapies.
引用
收藏
页码:9147 / 9168
页数:22
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