Review Article
Irisin: A Promising Target for Ischemia-Reperfusion Injury Therapy
Table 1
The effects and mechanisms of irisin during ischemia-reperfusion injury.
| Organs | Effects on IRI | Mechanisms involving irisin | Ref. |
| Cerebral IRI | Inflammation↓ | NLRP3 pathway | [119] | Inflammation↓ | Notch pathway | [120, 121] | O2•-↓, MDA↓, 4-HNEs↓ | PKB and ERK pathways | [97] | PGC1-α↑, TFAM↑ | Mitochondrial biogenesis | [113] | Flap revascularization | Endothelial cell proliferation | Antioxidative stress | [102] | Heart IRI | HDAC4 degradation↓ | HDAC sumoylation | [108] | MITOL↑ | Anti-ER stress | [122] | NOX↓ | Antioxidative stress | [100] | Opa1↑ | Mitochondrial fusion | [42] | Opa1↑ | Mitophagy | [76, 111] | PGC1-α deacetylation | AMPK pathway | [126, 127] | Proangiogenic function | ERK pathway | [129] | ROS↓, SOD↑ | Antioxidative stress | [95, 96] | SOD2↑, calcium overload↓ | Mitochondrial permeability | [95] | SOD2 localization | Mitochondrial permeability | [96] | UCP3↑ | Anti-mtROS | [107] | Hepatic IRI | Drp1↓, Fis1↓ | Mitochondrial fission | [68] | PGC1-α↑, TFAM↑ | Mitochondrial biogenesis | [68] | Kindlin-2↑ | Anti-ER stress | [125] | UCP2↑ | Anti-mtROS | [68] | Hind limb IRI | Inflammatory biomarkers↓ | Anti-inflammation | [118] | Intestinal IRI | Inflammation↓ | Anti-ER stress | [99] | MDAs↓, 4-HNEs↓, GPXs↑ | Antioxidative stress | [98] | SOD↑, GPXs↑, XO↓ | Antioxidative stress | [99] | Pulmonary IRI | UCP2↑ | Anti-mtROS | [105] | Renal IRI | Inflammation↓ | Anti-ER stress | [117] | Inflammation↓ | P53 inactivation | [117] | UCP2↑ | Anti-mtROS | [106] |
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AMPK: adenosine 5 -monophosphate-activated protein kinase; Drp1: dynamin-related protein 1; ERK: extracellular-regulated protein kinases; ER stress: endoplasmic reticulum stress; Fis1: fission protein 1; GPXs: glutathione peroxidases; HDAC: histone deacetylases; 4-HNEs: 4-hydroxy-2-nonenals; IRI: ischemia-reperfusion injury; MDAs: malondialdehydes; MMP: mitochondrial membrane potential; mPTP: mitochondrial permeability transition pore; mtROS: mitochondrial reactive oxygen species; NOX: NADPH oxidase; O 2•-: superoxide; Opa 1: optic atrophy 1; PGC1- α: PPAR-c coactivator-1 α; PKB: protein kinase B; SOD: superoxide dismutase; TFAM: target mitochondrial transcription factor A; UCPs: uncoupling proteins; XO: xanthine oxidase; ↑: increase; ↓: decrease; /: “or”. |