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Exploring Caspase Mutations and Post-Translational Modification by Molecular Modeling Approaches
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Caspase-1 as Molecular Key in Cardiac Remodeling during Cardiorenal Syndrome Type 3 in the Murine Model
Mayra Trentin-Sonoda1,2, Frayli Maltoni Fratoni1, Carolina Victoria da Cruz Junho1
1Center of Natural and Human Sciences (CCNH), Universidade Federal do ABC, Santo Andre, SP, Brazil.
Insights
Mice lacking caspase-1 showed increased cardiac hypertrophy after kidney injury. This suggests caspase-1 plays a role in protecting the heart from inflammation-induced damage, even independently of IL-1β.
Area of Science:
- Cardiovascular Research
- Renal Physiology
- Inflammatory Pathways
Background:
- Renal ischemia/reperfusion triggers systemic inflammation, contributing to cardiorenal syndrome type 3 and cardiac hypertrophy.
- Inflammasome activation and caspase-1-dependent IL-1β cleavage are implicated in cardiovascular diseases.
Purpose of the Study:
- To investigate the role of caspase-1 in cardiac hypertrophy and apoptosis following renal ischemia/reperfusion.
- To elucidate the impact of caspase-1 deficiency on the heart's response to renal injury.
Main Methods:
- Utilized wildtype and caspase-1 knockout mice subjected to a 60-minute renal ischemia and 15-day reperfusion protocol.
- Analyzed cardiac gene expression via Real-Time PCR and evaluated caspase activity.
Main Results:
- Absence of caspase-1 exacerbated cardiac hypertrophy in mice post-renal ischemia/reperfusion.
- The hypertrophic response was associated with elevated caspase-3/7 and caspase-9 activity, indicating apoptosis initiation independent of IL-1β.
Conclusions:
- Caspase-1 deficiency worsens cardiac hypertrophy following renal ischemia/reperfusion.
- The findings highlight caspase-1's crucial role in cardiac remodeling and protection, independent of IL-1β signaling.
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.
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