IL‐37 Modulates Myocardial Calcium Handling via the p‐STAT3/SERCA2a Axis in HF‐Related Engineered Human Heart Tissue

Author:

Yin Dan1ORCID,Liu Yong1,Xue Bingqing1,Ding Rui1,Wang Gang1,Xia Shutao1,Zhang Donghui1ORCID

Affiliation:

1. State Key Laboratory of Biocatalysis and Enzyme Engineering School of Life Science Hubei University Wuhan 430062 China

Abstract

AbstractInterleukin‐37 (IL‐37) is a potent anti‐inflammatory cytokine belonging to the IL‐1 family. This study investigates the regulatory mechanism and reparative effects of IL‐37 on HF‐related human induced pluripotent stem cells derived cardiomyocytes (hiPSC‐CMs) and engineered human heart tissue subjected to hypoxia and H2O2 treatment. The contractile force and Ca2+ conduction capacity of the tissue are assessed using a stretching platform and high‐resolution fluorescence imaging system. This investigation reveals that IL‐37 treatment significantly enhances cell viability, calcium transient levels, contractile force, and Ca2+ conduction capacity in HF‐related hiPSC‐CMs and engineered human heart tissue. Notably, IL‐37 facilitates the upregulation of sarcoplasmic reticulum calcium ATPase 2a (SERCA2a) through enhancing nuclear p‐STAT3 levels. This effect is mediated by the binding of p‐STAT3 to the SERCA2a promoter, providing a novel insight on the reparative potential of IL‐37 in HF. IL‐37 demonstrates its ability to enhance systolic function by modulating myocardial calcium handling via the p‐STAT3/SERCA2a axis in HF‐related engineered human heart tissue (as shown in schematic diagram).

Funder

National Key Research and Development Program of China

National Natural Science Foundation of China

Publisher

Wiley

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