Departamento de Ciencias Biomédicas, Centro Universitario de Tonalá, Universidad de Guadalajara, C.P. 45425, Tonalá, Jalisco, Mexico.
Departamento de Fisiología, Centro Universitario de Ciencias de la Salud, C.P. 44340, Guadalajara, Jalisco, Mexico.
Oxid Med Cell Longev. 2022 Apr 11;2022:8624318. doi: 10.1155/2022/8624318. eCollection 2022.
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.
缺血再灌注（I-R）损伤是指恢复缺血组织或器官血流时造成的损伤。这种复杂而特征性的损伤会加速细胞死亡，诱导细胞死亡的信号通路包括细胞凋亡、细胞坏死，甚至铁死亡。除了 I-R 与活性氧和活性氮释放之间的直接关联外，它还涉及线粒体氧化损伤的发展。因此，其机制通过活性物质清除、钙超载调节、电子传递链阻断、线粒体通透性转换孔激活或非编码 RNA 转录发挥关键作用。其他受体和分子可减轻这种病理和其他相关疾病引起的组织和器官损伤。这些分子靶点已逐渐被发现，在 I-R 缓解中具有重要作用。因此，本研究旨在强调这些发现的重要性。在这篇综述中，我们探讨了与减轻与 I-R 相关的氧化应激诱导的损伤相关的氧化损伤受体。尽管手术技术和病理学干预的一些并发症不能减轻 I-R 引起的损伤，但这些使用替代靶点开发的治疗方法可能作为组织移植或 I-R 相关病理学的辅助治疗。
