Table 1.
Functions of Irisin in CHD.
| Effect | Experimental Subjects | Detail | Reference |
|---|---|---|---|
| Reducing endothelial inflammation and oxidative stress | HUVECs | Activating AMPK-PI3K-Akt-enos signaling pathway | (65, 66) |
| HUVECs | Inhibiting p38 MAPK/NF-κB pathway | (67) | |
| HUVECs | Inhibiting PKC-β/NADPH oxidase | (68) | |
| HUVECs | Inhibiting ROS-NLRP3 inflammasome signaling | (70) | |
| HUVECs | Suppressing TNFα-induced VCAM-1 | (71) | |
| Promoting endothelial proliferation | HUVECs | Up-regulating microRNA126-5p | (69) |
| HUVECs | Up-regulating ERK signaling pathway and suppressing high glucose-induced apoptosis | (109) | |
| Reducing lipid accumulation in macrophages | RAW264.7 macrophages | Regulating Bcl-2, Bax and caspase-3 | (67) |
| HCAECs | Inhibiting the expression of hsCPR, ICAM-1 and E-selectin | (72) | |
| RAW264.7 macrophages | Inhibiting PERK/eif2α/CHOP and ATF6/CHOP ER pathways | (73) | |
| Protecting cardiomyocytes | H9c2 cells, mouse ESCs | Inducing HDAC4 degradation to protect mitochondria | (97, 100) |
| Primary cardiomyocytes | Activating mitochondrial autophagy | (86) | |
| H9c2 cells | Reducing the production of HO-induced ROS | (98) | |
| H9c2 cells | Inhibit the opening of mPTP | (99) | |
| H9c2 cells | Increasing the activity of SOD2 | (102) | |
| H9c2 cells | anti-oxidation by the AKT/GSK3β/FYN/Nrf2 axis | (49) | |
| H9c2 cells | Activating AMPK pathway | (110) | |
| Sprague–Dawley rats | Causing bradycardia to reduce the energy consumption | (87) | |
| Indicating the process of ACS | Rats or mice | Decreasing at acute phase after MI | (81, 82) |
| Patients | Decreasing at acute phase after MI | (76, 83–85) | |
| Inconsistencies in long-term monitoring of ACS | Patients | Increasing at 6 months after PCI | (53) |
| Patients | Lower in MI patients | (91) | |
| Patients | Positively correlating to CHD events after PCI | (77) | |
| Patients | A positive predictor of MACE after surgery | (83) | |
| Patients | Irisin genotypes be considered as genetic risk factors of MI | (93) | |
| Treating atherosclerosis | C57BL/6 mice, apoE-deficient mice | Improving EDV and reducing the area of atherosclerotic plaque | (66, 69) |
| apoE-deficient mice | Inhibiting the new carotid artery intima’s formation | (67, 69) | |
| Treating ACS | BM-MSCs | Enhancing the repairing effect in the process of cell transplantation of heart | (107) |
| C57BL/6 mice | Accelerating the restoration of infarcted area | (104, 107) | |
| FNDC5 knockout mice | Accelerating the restoration of infarcted area | (105) |
HUVEC, human coronary artery endothelial cell; ROS, reactive oxygen species; mPTP, mitochondrial permeability transition pore; SOD2, superoxide dismutase 2; MI, myocardial infarction; CHD, coronary heart disease; PCI, percutaneous coronary intervention; MACE, major adverse cardiovascular events; EDV, endothelium-dependent dilation function; apoE, apolipoprotein E; BM-MSC, bone marrow-derived mesenchymal stem cell.