Protective molecular mechanisms of clusterin against apoptosis in cardiomyocytes

Autor(es)

Pereira, Rodrigo Martins ^{[1, 2]} ; Mekary, Rania A. ^{[3, 4]} ; da Cruz Rodrigues, Kellen Cristina ^{[1, 2]} ; Anaruma, Chadi Pellegrini ^{[1, 2]} ; Ropelle, Eduardo Rochete ^{[1, 2]} ; Ramos da Silva, Adelino Sanchez ^[5] ; Cintra, Dennys Esper ^[1] ; Pauli, Jose Rodrigo ^{[1, 2]} ; de Moura, Leandro Pereira ^{[1, 2]}

Afiliação do(s) autor(es)

^[1] Univ Estadual Campinas, Sch Appl Sci, Lab Mol Biol Exercise LaBMEx, 1300 Pedro Zaccaria St, Sao Paulo - Brazil

^[2] Univ Campinas UNICAMP, Sch Appl Sci, CEPECE Ctr Res Sport Sci, Sao Paulo - Brazil

^[3] MCPHS Univ, Dept Pharmaceut Business & Adm Sci, Boston, MA - USA

^[4] Harvard Med Sch, Brigham & Womens Hosp, Dept Surg, Boston, MA - USA

^[5] Univ Sao Paulo, Sch Phys Educ & Sport Ribeiro Preto, Sao Paulo - Brazil

• Tipo de documento: Artigo de Revisão
• Fonte: HEART FAILURE REVIEWS; v. 23, n. 1, p. 123-129, JAN 2018.
• Citações Web of Science: 6

Resumo

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. (AU)

• Processo FAPESP: 15/07199-2 - Papel da clusterina/ApoJ na sinalização da insulina em resposta ao exercício físico em roedores e em humanos
• Beneficiário: Leandro Pereira de Moura
• Modalidade de apoio: Auxílio à Pesquisa - Jovens Pesquisadores
• Processo FAPESP: 16/12569-6 - Efeitos de diferentes intensidades do exercício físico no metabolismo da clusterina e sua interferência na sinalização da insulina em roedores
• Beneficiário: Rodrigo Martins Pereira
• Modalidade de apoio: Bolsas no Brasil - Doutorado Direto