Your browser doesn't support javascript.
loading
Physiological and cellular mechanisms of ischemic preconditioning microRNAs-mediated in underlying of ischemia/reperfusion injury in different organs.
Gheitasi, Izadpanah; Akbari, Ghaidafeh; Savari, Feryal.
Afiliação
  • Gheitasi I; Department of Physiology, Faculty of Medicine, Yasuj University of Medical Sciences, Yasuj, Iran.
  • Akbari G; Department of Physiology, Faculty of Medicine, Yasuj University of Medical Sciences, Yasuj, Iran. akbari8836@gmail.com.
  • Savari F; Department of Medical Basic Sciences, Shoushtar Faculty of Medical Sciences, Shoushtar, Iran. feryal.savari@gmail.com.
Mol Cell Biochem ; 2024 Jul 13.
Article em En | MEDLINE | ID: mdl-39001984
ABSTRACT
Ischemia-reperfusion (I/R) injury, as a pathological phenomenon, takes place when blood supply to an organ is disrupted and then aggravated during restoration of blood flow. Ischemic preconditioning (IPC) is a potent method for attenuating subsequent events of IR damage in numerous organs. IPC protocol is determined by a brief and sequential time periods of I/R before the main ischemia. MicroRNAs are endogenous non-coding RNAs that regulate post-transcriptionally target mRNA translation via degrading it and/or suppressing protein synthesis. This review introduces the physiological and cellular mechanisms of ischemic preconditioning microRNAs-mediated after I/R insult in different organs such as the liver, kidney, heart, brain, and intestine. Data of this review have been collected from the scientific articles published in databases such as Science Direct, Scopus, PubMed, Web of Science, and Scientific Information Database from 2000 to 2023. Based on these literature studies, IPC/IR intervention can affect cellular mechanisms including oxidative stress, apoptosis, angiogenesis, and inflammation through up-regulation or down-regulation of multiple microRNAs and their target genes.
Palavras-chave

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Ano de publicação: 2024 Tipo de documento: Article