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Therapeutic Targets for Regulating Oxidative Damage Induced by Ischemia-Reperfusion Injury: A Study from a Pharmacological Perspective

Authors :
Walter Ángel Trujillo-Rangel
Leonel García-Valdés
Miriam Méndez-del Villar
Rolando Castañeda-Arellano
Sylvia Elena Totsuka-Sutto
Leonel García-Benavides
Source :
Oxidative Medicine and Cellular Longevity. 2022:1-25
Publication Year :
2022
Publisher :
Hindawi Limited, 2022.

Abstract

Ischemia-reperfusion (I-R) injury is damage caused by restoring blood flow into ischemic tissues or organs. This complex and characteristic lesion accelerates cell death induced by signaling pathways such as apoptosis, necrosis, and even ferroptosis. In addition to the direct association between I-R and the release of reactive oxygen species and reactive nitrogen species, it is involved in developing mitochondrial oxidative damage. Thus, its mechanism plays a critical role via reactive species scavenging, calcium overload modulation, electron transport chain blocking, mitochondrial permeability transition pore activation, or noncoding RNA transcription. Other receptors and molecules reduce tissue and organ damage caused by this pathology and other related diseases. These molecular targets have been gradually discovered and have essential roles in I-R resolution. Therefore, the current study is aimed at highlighting the importance of these discoveries. In this review, we inquire about the oxidative damage receptors that are relevant to reducing the damage induced by oxidative stress associated with I-R. Several complications on surgical techniques and pathology interventions do not mitigate the damage caused by I-R. Nevertheless, these therapies developed using alternative targets could work as coadjuvants in tissue transplants or I-R-related pathologies

Details

ISSN :
19420994 and 19420900
Volume :
2022
Database :
OpenAIRE
Journal :
Oxidative Medicine and Cellular Longevity
Accession number :
edsair.doi.dedup.....c12a9187b3a578bed4fed62a52a70815