dc.contributor.author | Ghaderi, S | |
dc.contributor.author | Alidadiani, N | |
dc.contributor.author | Dilaver, N | |
dc.contributor.author | Heidari, HR | |
dc.contributor.author | Parvizi, R | |
dc.contributor.author | Rahbarghazi, R | |
dc.contributor.author | Soleimani-Rad, J | |
dc.contributor.author | Baradaran, B | |
dc.date.accessioned | 2018-08-26T09:34:08Z | |
dc.date.available | 2018-08-26T09:34:08Z | |
dc.date.issued | 2017 | |
dc.identifier.uri | http://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/57694 | |
dc.description.abstract | Glycogen synthase kinase-3 beta (GSK3?) is principally is a glycogen synthase phosphorylating enzyme that is well known for its role in muscle metabolism. GSK3? is a serine/threonine protein Kinase, which is responsible for several essential roles in mammalian cells. This enzyme is implicated in the pathophysiology of many conditions involved in homeostasis and cellular immigration. GSK3? is involved in several pathways leading to neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. Increasing evidence has shown the potential importance of GSK3? in ischemic heart disease and ischemia-reperfusion pathologies. Reperfusion injury may occur in tissues after prolonged ischemia following reperfusion. Reperfusion injury can be life threatening. Reperfusion injury occurs due to a change in ionic homeostasis, excess free radical production, mitochondrial damage and cell death. There are however clear, cardiac-protective signals; although the molecular pathophysiology is not clearly understood. In normal physiology, GSK3? has a critical role in the cytoprotective pathway. However, it`s controversial role in ischemia and ischemia-reperfusion is a topic of current interest. In this review, we have opted to focus on GSK3? interactions with mitochondria in ischemic heart disease and expand on the therapeutic interventions. © 2017, Springer Science+Business Media New York. | |
dc.language.iso | English | |
dc.relation.ispartof | Apoptosis | |
dc.subject | 1,2,3,6 tetrahydro 1 methyl 4 phenylpyridine | |
dc.subject | adenosine triphosphate | |
dc.subject | casein kinase I | |
dc.subject | glycogen synthase kinase 3beta | |
dc.subject | mitochondrial permeability transition pore | |
dc.subject | mitogen activated protein kinase p38 | |
dc.subject | phosphatidylinositol 4,5 bisphosphate 3 kinase | |
dc.subject | protein kinase B | |
dc.subject | reactive oxygen metabolite | |
dc.subject | serum response factor | |
dc.subject | somatomedin | |
dc.subject | glycogen synthase kinase 3beta | |
dc.subject | GSK3B protein, human | |
dc.subject | protein kinase B | |
dc.subject | acidosis | |
dc.subject | heart infarction | |
dc.subject | heart muscle metabolism | |
dc.subject | human | |
dc.subject | mitochondrial membrane | |
dc.subject | mitochondrial membrane potential | |
dc.subject | mitochondrion | |
dc.subject | myocardial ischemia reperfusion injury | |
dc.subject | priority journal | |
dc.subject | Review | |
dc.subject | signal transduction | |
dc.subject | Wnt signaling pathway | |
dc.subject | apoptosis | |
dc.subject | cardiac muscle cell | |
dc.subject | enzymology | |
dc.subject | genetics | |
dc.subject | heart infarction | |
dc.subject | pathophysiology | |
dc.subject | phosphorylation | |
dc.subject | reperfusion injury | |
dc.subject | skeletal muscle | |
dc.subject | Apoptosis | |
dc.subject | Glycogen Synthase Kinase 3 beta | |
dc.subject | Humans | |
dc.subject | Mitochondria | |
dc.subject | Muscle, Skeletal | |
dc.subject | Myocardial Infarction | |
dc.subject | Myocytes, Cardiac | |
dc.subject | Phosphorylation | |
dc.subject | Proto-Oncogene Proteins c-akt | |
dc.subject | Reperfusion Injury | |
dc.subject | Signal Transduction | |
dc.title | Role of glycogen synthase kinase following myocardial infarction and ischemia-reperfusion | |
dc.type | Article | |
dc.citation.volume | 22 | |
dc.citation.issue | 7 | |
dc.citation.spage | 887 | |
dc.citation.epage | 897 | |
dc.citation.index | Scopus | |
dc.identifier.DOI | https://doi.org/10.1007/s10495-017-1376-0 | |