Mayra Trentin-Sonoda1,2, Frayli Maltoni Fratoni1, Carolina Victoria da Cruz Junho1, Wellington Caio Silva1, Karine Panico1, Marcela Sorelli Carneiro-Ramos1.
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-1β 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-1β- independent manner.
CONCLUSION: Our data corroborate important findings on the role of caspase-1 in the development of cardiac hypertrophy and remodeling. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.
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-1β 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-1β- independent manner.
CONCLUSION: Our data corroborate important findings on the role of caspase-1 in the development of cardiac hypertrophy and remodeling. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.
Entities:
Keywords:
Apoptosis; cardiac hypertrophy; cardiorenal syndrome; caspase-1; inflammation; renal injury.
Year: 2019
PMID： 31526348 DOI： 10.2174/1566524019666190916153257
Source DB: PubMed Journal: Curr Mol Med ISSN： 1566-5240 Impact factor: 2.222