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Interleukin-33 Mediates Cardiomyopathy After Acute Kidney Injury by Signaling to Cardiomyocytes
Nans Florens1, Rajesh K Kasam1, Valeria Rudman-Melnick1
1Department of Pediatrics, Cincinnati Children's Hospital Medical Center, OH (N.F., R.K.K., V.R.-M., S.-C.L., V.P., J.D.M.).
Circulation
|January 25, 2023
Summary
Interleukin-33 (IL-33) released during acute kidney injury (AKI) directly causes heart problems. Blocking the IL-33/ST2L pathway protects the heart, suggesting a new treatment for cardiorenal syndrome.
Area of Science:
- Cardiorenal Medicine
- Molecular Cardiology
- Renal Pathophysiology
Background:
- Acute kidney injury (AKI) is a critical condition that can lead to chronic kidney disease and cardiac complications like hypertrophy and cardiomyopathy.
- The interplay between kidney injury and cardiac remodeling is complex and not fully understood.
Purpose of the Study:
- To investigate the role of interleukin-33 (IL-33) and its receptor ST2L in cardiac remodeling following acute kidney injury (AKI).
- To explore the therapeutic potential of targeting the IL-33/ST2L axis for cardiorenal protection.
Main Methods:
- Utilized mouse models of ischemia/reperfusion AKI and unilateral ureteral obstruction.
- Employed genetic disruption of the IL-33/ST2L axis in specific cell types.
- Administered IL-33 monoclonal antibody, adeno-associated virus vectors for IL-33 or ST2L, and recombinant IL-33.
Main Results:
- Mice lacking IL-33 were protected from AKI-induced cardiomyopathy.
- IL-33 monoclonal antibody treatment attenuated cardiac remodeling post-AKI.
- IL-33 overexpression induced cardiac hypertrophy, dependent on ST2L expression in cardiac myocytes.
Conclusions:
- Kidney-derived IL-33 directly contributes to cardiorenal syndrome by acting on cardiac myocytes.
- Antagonizing the IL-33/ST2L axis shows promise as a cardioprotective strategy in kidney disease patients.
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