Irisin: A Promising Target for Ischemia-Reperfusion Injury Therapy.
Yani WangHuibin LiuNa SunJing LiXiang PengYing JiaJason KarchBo YuXander H T WehrensJinwei TianPublished in: Oxidative medicine and cellular longevity (2021)
Ischemia-reperfusion injury (IRI) is defined as the total combined damage that occurs during a period of ischemia and following the recovery of blood flow. Oxidative stress, mitochondrial dysfunction, and an inflammatory response are factors contributing to IRI-related damage that can each result in cell death. Irisin is a polypeptide that is proteolytically cleaved from the extracellular domain of fibronectin type III domain-containing protein 5 (FNDC5). Irisin acts as a myokine that potentially mediates beneficial effects of exercise by reducing oxidative stress, improving mitochondrial fitness, and suppressing inflammation. The existing literature also suggests a possible link between irisin and IRI, involving mechanisms similar to those associated with exercise. This article will review the pathogenesis of IRI and the potential benefits and current limitations of irisin as a therapeutic strategy for IRI, while highlighting the mechanistic correlations between irisin and IRI.
Keyphrases
- oxidative stress
- ischemia reperfusion injury
- blood flow
- type iii
- inflammatory response
- diabetic rats
- cell death
- dna damage
- induced apoptosis
- physical activity
- systematic review
- signaling pathway
- toll like receptor
- climate change
- mesenchymal stem cells
- small molecule
- human health
- heat shock protein
- replacement therapy