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[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.
Wen, Ri; Zhang, Tie-Ning; Yang, Ni.
Afiliação
  • Wen R; Department of Pediatric Intensive Care Unit, Shengjing Hospital, China Medical University, Shenyang 110004, China.
  • Zhang TN; Department of Pediatric Intensive Care Unit, Shengjing Hospital, China Medical University, Shenyang 110004, China.
  • Yang N; Department of Pediatric Intensive Care Unit, Shengjing Hospital, China Medical University, Shenyang 110004, China.
Zhongguo Dang Dai Er Ke Za Zhi ; 26(7): 774-781, 2024 Jul 15.
Article em Zh | MEDLINE | ID: mdl-39014956
ABSTRACT
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.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Sepse / Piroptose Limite: Animals / Humans Idioma: Zh Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Sepse / Piroptose Limite: Animals / Humans Idioma: Zh Ano de publicação: 2024 Tipo de documento: Article