Key result
Targeting the HSP90β/HAX-1 interaction enhances cardiomyocyte contractility, calcium kinetics, and cell survival under stress.
Why the study?
Does an interfering peptide targeting HSP90β/HAX-1 interaction improve contractility and survival in human iPSC-derived cardiomyocytes under stress?
Population
Cardiomyocytes derived from human induced pluripotent stem cells
Design
Preclinical
Authors
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Targeting the HSP90β/HAX-1 interaction at the ER/SR compartment with an interfering peptide may serve as a novel strategy to enhance cardioprotection and contractility under stress.
Does an interfering peptide targeting HSP90β/HAX-1 interaction improve contractility and survival in human iPSC-derived cardiomyocytes under stress?
Targeting the HSP90β/HAX-1 interaction at the ER/SR compartment with an interfering peptide may serve as a novel strategy to enhance cardioprotection and contractility under stress.
Sen et al. (2025) studied Cardiac disease and stress. HSP90β/HAX-1 interfering peptide was evaluated on Contractility, calcium kinetics, and cell viability under stress. An ER/SR-targeted interfering peptide disrupting HSP90β/HAX-1 interaction significantly enhanced contractility, calcium kinetics, and cardiomyocyte survival under stress in vitro.
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