TY - JOUR
T1 - Mg53 protein protects against multiorgan ischemia/reperfusion injury
T2 - Present and future
AU - Liu, Teng Fei
AU - Zhou, Jian Kang
AU - Huang, Tuan Jie
AU - Xing, Qu
AU - Cheng, Kang
AU - Li, Peng
AU - Li, Dong Peng
AU - Yang, Bo
AU - Ma, Shan Shan
AU - Guan, Fang Xia
N1 - Funding Information:
BACKGROUND: In recent years, with the progress of shock therapy as well as the establishment and promoted application of arterial bypass grafting, thrombolytic therapy, percutaneous transluminal coronary angioplasty, extracorporeal circulation on cardiac surgery, cardiopulmonary resuscitation, limb replantation, and organ transplantation, blood reperfusion in multiple organs after ischemia has been achieved. However, the organs which undergo a period of ischemia appear to have the performance of damage aggravation. OBJECTIVE: To summarize the research progress of MG53 protein in protecting five organs from ischemia/reperfusion injury, thereby providing reference for further in-depth study. METHODS: A computer-based online search of PubMed, Duxiu Knowledge Search and CNKI databases was performed for relevant literatures puldished between 1986 and 2016. The key words were “MG53, TRIM, Mitsugumin53, ischemic, reperfusion, preconditioning, postconditioning, RISK, membrane damage, Connexin43, KChIP2” in English and “MG53, ischemia/reperfusion” in Chinese. Finally 61 eligible articles were reviewed in accordance with the inclusion and exclusion criteria. RESULTS AND CONCLUSION: As a muscle-specific TRIM family protein, endogenous MG53 is involved in the repair of muscle cytomembrane damage, and the protective effects of ischemic preconditioning and postconditioning. Exogenous recombinant human MG 53 protein not only repairs membrane damage of various muscles and non-muscle cells, but also protects the myocardium, skeletal muscle, brain, lung and kidney from ischemia/reperfusion injury. Subject headings: Muscles; Blood Vessels; Ischemia; Organ Transplantation; Tissue Engineering Funding: The National Natural Science Foundation of China, No. 81601078 and 81471306; the Science & Technology Innovation Foundation for Higher Education Institutes of Henan Province of China, No. 15IRTSTHN022; the Plan for Scientific Innovation Talent of Henan Province, No. 154200510008; the International Cooperation Project of Henan Province of China, No. 2016GH03 and 2016GH15
Publisher Copyright:
© 2017, Journal of Clinical Rehabilitative Tissue Engineering Research. All Rights Reserved.
PY - 2017
Y1 - 2017
N2 - Background: In recent years, with the progress of shock therapy as well as the establishment and promoted application of arterial bypass grafting, thrombolytic therapy, percutaneous transluminal coronary angioplasty, extracorporeal circulation on cardiac surgery, cardiopulmonary resuscitation, limb replantation, and organ transplantation, blood reperfusion in multiple organs after ischemia has been achieved. However, the organs which undergo a period of ischemia appear to have the performance of damage aggravation. Objective: To summarize the research progress of MG53 protein in protecting five organs from ischemia/reperfusion injury, thereby providing reference for further in-depth study. METHODS: A computer-based online search of PubMed, Duxiu Knowledge Search and CNKI databases was performed for relevant literatures puldished between 1986 and 2016. The key words were “MG53, TRIM, Mitsugumin53, ischemic, reperfusion, preconditioning, postconditioning, RISK, membrane damage, Connexin43, KChIP2” in English and “MG53, ischemia/reperfusion” in Chinese. Finally 61 eligible articles were reviewed in accordance with the inclusion and exclusion criteria. Results and Conclusion: As a muscle-specific TRIM family protein, endogenous MG53 is involved in the repair of muscle cytomembrane damage, and the protective effects of ischemic preconditioning and postconditioning. Exogenous recombinant human MG 53 protein not only repairs membrane damage of various muscles and non-muscle cells, but also protects the myocardium, skeletal muscle, brain, lung and kidney from ischemia/reperfusion injury.
AB - Background: In recent years, with the progress of shock therapy as well as the establishment and promoted application of arterial bypass grafting, thrombolytic therapy, percutaneous transluminal coronary angioplasty, extracorporeal circulation on cardiac surgery, cardiopulmonary resuscitation, limb replantation, and organ transplantation, blood reperfusion in multiple organs after ischemia has been achieved. However, the organs which undergo a period of ischemia appear to have the performance of damage aggravation. Objective: To summarize the research progress of MG53 protein in protecting five organs from ischemia/reperfusion injury, thereby providing reference for further in-depth study. METHODS: A computer-based online search of PubMed, Duxiu Knowledge Search and CNKI databases was performed for relevant literatures puldished between 1986 and 2016. The key words were “MG53, TRIM, Mitsugumin53, ischemic, reperfusion, preconditioning, postconditioning, RISK, membrane damage, Connexin43, KChIP2” in English and “MG53, ischemia/reperfusion” in Chinese. Finally 61 eligible articles were reviewed in accordance with the inclusion and exclusion criteria. Results and Conclusion: As a muscle-specific TRIM family protein, endogenous MG53 is involved in the repair of muscle cytomembrane damage, and the protective effects of ischemic preconditioning and postconditioning. Exogenous recombinant human MG 53 protein not only repairs membrane damage of various muscles and non-muscle cells, but also protects the myocardium, skeletal muscle, brain, lung and kidney from ischemia/reperfusion injury.
KW - Blood vessels
KW - Ischemia
KW - Muscles
KW - Organ transplantation
KW - Tissue engineering
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U2 - 10.3969/j.issn.2095-4344.2017.20.021
DO - 10.3969/j.issn.2095-4344.2017.20.021
M3 - Article
AN - SCOPUS:85032035187
SN - 1673-8225
VL - 21
SP - 3248
EP - 3254
JO - Chinese Journal of Tissue Engineering Research
JF - Chinese Journal of Tissue Engineering Research
IS - 20
M1 - 2095-4344(2017)20-03248-07
ER -