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Protective molecular mechanisms of clusterin against apoptosis in cardiomyocytes

期刊

HEART FAILURE REVIEWS
卷 23, 期 1, 页码 123-129

出版社

SPRINGER
DOI: 10.1007/s10741-017-9654-z

关键词

Clusterin; Apolipoprotein J; Megalin; Apoptosis; Cardiomyocytes

资金

  1. Fundacao de Amparo a Pesquisa do Estado de Sao Paulo [2015/07199-2, 2016/12569-6]
  2. FAEPEX
  3. Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [15/07199-2] Funding Source: FAPESP

向作者/读者索取更多资源

Loss of cardiomyocytes occurs with aging and contributes to cardiovascular complications. In the present study, we highlighted the role of clusterin, a protein that has recently been associated with the protection of cardiomyocytes from apoptosis. Clusterin protects cardiac cells against damage from myocardial infarction, transplant, or myocarditis. Clusterin can act directly or indirectly on apoptosis by regulating several intracellular pathways. These pathways include (1) the oxidant and inflammatory program, (2) insulin growth factor 1 (IGF-1) pathway, (3) KU70 / BCL-2-associated X protein (BAX) pathway, (4) tumor necrosis factor alpha (TNF-alpha) pathway, (5) BCL-2 antagonist of cell death (BAD) pathway, and (6) mitogen-activated protein kinase (MAPK) pathway. Given the key role of clusterin in preventing loss of cardiac tissue, modulating the expression and function of this protein carries the potential of improving cardiovascular care in the future.

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