泛凋亡对心力衰竭的潜在治疗前景

IF 4.2 2区 医学 Q2 IMMUNOLOGY Journal of Inflammation Research Pub Date : 2024-11-19 eCollection Date: 2024-01-01 DOI:10.2147/JIR.S485901
Yunfeng Jia, Yayi Liu, Yiming Zuo, Junping Zhang, Yanyang Li, Xuezheng Liu, Shichao Lv
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引用次数: 0

摘要

心力衰竭(HF)是各种心脏疾病的严重表现或晚期阶段。心力衰竭继续给全球带来沉重的疾病负担,住院率和死亡率都很高。此外,人们对心力衰竭的发病机理和病理生理过程仍然知之甚少,使其预防和治疗策略变得更加复杂。与心房颤动相关的一个重要病理生理机制是全身炎症反应。PAN凋亡是一种新型的炎症细胞死亡模式,已在感染性疾病、神经退行性疾病、癌症和其他炎症病症中得到广泛研究。最近的研究发现,在高频样本中,与 PANoptosis 相关的基因明显失调。因此,PAN凋亡介导的炎症反应可能是高频的潜在机制和治疗靶点。本文全面分析了驱动 PAN 细胞凋亡的分子途径。我们讨论了 PAN 细胞凋亡在高血脂中的作用和潜在治疗靶点,从而为临床治疗和新型疗法的开发提供有价值的见解。
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The Potential Therapeutic Prospect of PANoptosis in Heart Failure.

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.

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来源期刊
Journal of Inflammation Research
Journal of Inflammation Research Immunology and Microbiology-Immunology
CiteScore
6.10
自引率
2.20%
发文量
658
审稿时长
16 weeks
期刊介绍: An international, peer-reviewed, open access, online journal that welcomes laboratory and clinical findings on the molecular basis, cell biology and pharmacology of inflammation.
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