Caspase-1 as Molecular Key in Cardiac Remodeling during Cardiorenal Syndrome Type 3 in the Murine Model

Autor(es)

Trentin-Sonoda, Mayra ^{[1, 2]} ; Fratoni, Frayli Maltoni ^[1] ; da Cruz Junho, Carolina Victoria ^[1] ; Silva, Wellington Caio ^[1] ; Panico, Karine ^[1] ; Carneiro-Ramos, Marcela Sorelli ^[1]

Afiliação do(s) autor(es)

^[1] Univ Fed ABC, Ctr Nat & Human Sci CCNH, Santo Andre, SP - Brazil

^[2] Univ Ottawa, Fac Med, Cellular & Mol Med, Ottawa, ON - Canada

• Tipo de documento: Artigo Científico
• Fonte: CURRENT MOLECULAR MEDICINE; v. 20, n. 1, p. 72-78, 2020.
• Citações Web of Science: 0

Resumo

Background: Renal ischemia/reperfusion induces a systemic inflammatory response that is directly related to the development of cardiac hypertrophy due to cardiorenal syndrome type 3. Classic inflammatory pathways have been extensively investigated in cardiovascular diseases, including the participation of inflammasome in caspase-1-dependent IL-1 beta cleavage. Objective: In this study, we aimed to understand how lack of caspase-1 would impact the hypertrophic and apoptotic response in the heart after renal ischemia/reperfusion. Methods: Wildtype and caspase-1 knockout animals were submitted to a renal ischemia/reperfusion protocol. Briefly, left kidney ischemia was induced in male C57BL/6 mice for 60 min, followed by reperfusion for 15 days. Gene expression was analysed by Real-Time PCR. Caspase activity was also evaluated. Results: Lack of caspase-1 led to a more pronounced cardiac hypertrophy in mice subjected to renal ischemia-reperfusion. Such hypertrophic process was accompanied by increased activity of caspase3/7 and 9, indicating apoptosis initiation in an IL-1 beta-independent manner. Conclusion: Our data corroborate important findings on the role of caspase-1 in the development of cardiac hypertrophy and remodeling. (AU)

• Processo FAPESP: 15/15832-7 - Impacto da insuficiência renal no tecido cardíaco in vivo: contribuição da apoptose celular no remodelamento cardíaco
• Beneficiário: Frayli Maltoni Fratoni
• Modalidade de apoio: Bolsas no Brasil - Iniciação Científica
• Processo FAPESP: 15/19107-5 - TLR4 e sistema complemento: possível mecanismo chave na resposta hipertrófica do tecido cardíaco em quadro inflamatório sistêmico induzido por lesão isquêmica renal
• Beneficiário: Marcela Sorelli Carneiro Ramos
• Modalidade de apoio: Auxílio à Pesquisa - Regular