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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

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

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Author(s):
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]
Total Authors: 6
Affiliation:
[1] Univ Fed ABC, Ctr Nat & Human Sci CCNH, Santo Andre, SP - Brazil
[2] Univ Ottawa, Fac Med, Cellular & Mol Med, Ottawa, ON - Canada
Total Affiliations: 2
Document type: Journal article
Source: CURRENT MOLECULAR MEDICINE; v. 20, n. 1, p. 72-78, 2020.
Web of Science Citations: 0
Abstract

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)

FAPESP's process: 15/15832-7 - Impact of the renal insufficiency in the in vivo cardiac tissue: contribution of cell apoptosis in cardiac remodeling
Grantee:Frayli Maltoni Fratoni
Support Opportunities: Scholarships in Brazil - Scientific Initiation
FAPESP's process: 15/19107-5 - TLR4 and complement system : possible key mechanism in renal ischemia/reperfusion induced cardiac hypertrophy
Grantee:Marcela Sorelli Carneiro Ramos
Support Opportunities: Regular Research Grants