The research of HSPB1 in apoptosis,autophagy and cardiogenic shock
作者机构：Hunan provincial key laboratory of emergency and critical care metabonomicsHunan provincial peoples hospital(The first affiliated hospital of Hunan normal university) The first affiliated hospital of Hunan normal universityChangshaChina
出 版 物：《实用休克杂志（中英文）》 (Journal of Practical Shock)
年 卷 期：2023年第7卷第6期
页 面：380-384页
主 题：Cardiogenic shock Acute myocardial infarction HSPB1 Endothelial cells Cardiac muscle cells Apoptosis Autophagy
摘 要：Cardiogenic shock(CS)is a common cause of mortality and treatment remains challenging despite advances in therapeutic options.CS is caused by severe impairment of myocardial performance that results in decreased cardiac output,hypoperfusion of the end organ,and hypoxia.Clinically this presents as hypotension refractory to volume resuscitation with features of end-organ hypoperfusion requiring pharmacological or mechanical intervention.Acute myocardial infarction(AMI)accounts for 81%of patients with CS.Heat shock protein family B member 1(HSPB1)is a multifunctional protein induced by various stress factors and has a protective effect on cells.A large number of studies have demonstrated that HSPB1 plays an important role in regulating apoptosis.Recently,some studies have suggested that HSPB1 also participates in the autophagic process.HSPB1 are expressed in many cells of the cardiovascular system such as endothelial cells,cardiac muscle cells,monocytes,and platelets.They are up-regulated in response to inflammation,oxidative stress,or ischemia and protect cells against extracellular stress factors.Here,we explore the involvement of HSPB1 in apoptosis,autophagy,and CS.We speculate that HSPB1 may exert its anti-myocardial injury role via the regulation of apoptosis and autophagy;this may provide the basis for the development of new approaches for the prevention and treatment of CS.
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