[Recent research on pyroptosis in sepsis-induced myocardial depression].
细胞焦亡在脓毒症心肌抑制中的作用研究进展.
Myocardial depression
Pyroptosis
Sepsis
Journal
Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
ISSN: 1008-8830
Titre abrégé: Zhongguo Dang Dai Er Ke Za Zhi
Pays: China
ID NLM: 100909956
Informations de publication
Date de publication:
15 Jul 2024
15 Jul 2024
Historique:
medline:
17
7
2024
pubmed:
17
7
2024
entrez:
17
7
2024
Statut:
ppublish
Résumé
Sepsis-induced myocardial depression (SIMD), a common complication of sepsis, is one of the main causes of death in patients with sepsis. The pathogenesis of SIMD is complicated, and the process of SIMD remains incompletely understood, with no single or definitive mechanism fully elucidated. Notably, pyroptosis, as a pro-inflammatory programmed cell death, is characterized by Gasdermin-mediated formation of pores on the cell membrane, cell swelling, and cell rupture accompanied by the release of large amounts of inflammatory factors and other cellular contents. Mechanistically, pyroptosis is mainly divided into the canonical pathway mediated by caspase-1 and the non-canonical pathway mediated by caspase-4/5/11. Pyroptosis has been confirmed to participate in various inflammation-associated diseases. In recent years, more and more studies have shown that pyroptosis is also involved in the occurrence and development of SIMD. This article reviews the molecular mechanisms of pyroptosis and its research progress in SIMD, aiming to provide novel strategies and targets for the treatment of SIMD. 脓毒症心肌抑制是脓毒症患者常见的并发症，是脓毒症患者死亡的主要原因之一。其发病机制复杂，目前尚无统一定论。细胞焦亡是一种促炎的程序性细胞死亡，其特点是Gasdermins家族介导的细胞膜孔洞形成、细胞肿胀、细胞破裂，伴随大量炎症因子等细胞内容物的释放。细胞焦亡在多种炎症相关疾病中扮演了重要角色，主要通过胱天蛋白酶（caspase）-1介导的经典通路和caspase-4/5/11介导的非经典通路发挥作用。越来越多的研究表明细胞焦亡参与脓毒症心肌抑制的发生发展。该文围绕细胞焦亡的分子学机制及其在脓毒症心肌抑制中的研究进展进行综述，以期为脓毒症心肌抑制的治疗提供新策略与新靶点。.
Autres résumés
Type: Publisher
(chi)
脓毒症心肌抑制是脓毒症患者常见的并发症，是脓毒症患者死亡的主要原因之一。其发病机制复杂，目前尚无统一定论。细胞焦亡是一种促炎的程序性细胞死亡，其特点是Gasdermins家族介导的细胞膜孔洞形成、细胞肿胀、细胞破裂，伴随大量炎症因子等细胞内容物的释放。细胞焦亡在多种炎症相关疾病中扮演了重要角色，主要通过胱天蛋白酶（caspase）-1介导的经典通路和caspase-4/5/11介导的非经典通路发挥作用。越来越多的研究表明细胞焦亡参与脓毒症心肌抑制的发生发展。该文围绕细胞焦亡的分子学机制及其在脓毒症心肌抑制中的研究进展进行综述，以期为脓毒症心肌抑制的治疗提供新策略与新靶点。.
Identifiants
pubmed: 39014956
pii: 1008-8830(2024)07-0774-08
doi: 10.7499/j.issn.1008-8830.2312039
pii:
doi:
Types de publication
Journal Article
Review
English Abstract
Langues
chi
Sous-ensembles de citation
IM
Pagination
774-781Références
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