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Protective molecular mechanisms of clusterin against apoptosis in cardiomyocytes

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Abstract

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-α) 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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Acknowledgements

We would like to thank the Brazilian foundations Fundação de Amparo à Pesquisa do Estado de São Paulo and FAEPEX for their indispensable support.

Funding

This work was supported by Fundação de Amparo à Pesquisa do Estado de São Paulo (grant numbers: 2015/07199-2 and 2016/12569-6) and FAEPEX.

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Correspondence to Leandro Pereira de Moura.

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Pereira, R.M., Mekary, R.A., da Cruz Rodrigues, K.C. et al. Protective molecular mechanisms of clusterin against apoptosis in cardiomyocytes. Heart Fail Rev 23, 123–129 (2018). https://doi.org/10.1007/s10741-017-9654-z

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