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-
Conclusion: Our data corroborate important findings on the role of caspase-1 in the
development of cardiac hypertrophy and remodeling.