Key result
Protein Kinase A modulates microtubule repolymerization in novel hiPSC-CM models of HCM.
Why the study?
How increased levels of α-tubulin and its post-translational modifications occur and may underlie cardiac dysfunction in human heart failure remains unknown, and the role of upstream kinases has not been explored.
PKA-microtubule modulation may offer a new HCM therapeutic axis; leaves open clinical translation from hiPSC models.
Background and aims: Increased levels of α-tubulin and its post-translational modifications (PTMs) are found in human heart failure and could initiate diastolic dysfunction by modulating cardiomyocyte stiffness. How these modifications occur and how they may underlie cardiac dysfunction remains unknown. Upstream kinases may play a critical role, but this has not been explored. Methods and results: as potential MT modifiers in HCM. Conclusions: created with BioRender.com.
No takes yet. Share an insight, caveat, or question.
Algul et al. (2026) studied Hypertrophic Cardiomyopathy. Protein Kinase A was identified as a modulator of microtubule repolymerization in hypertrophic cardiomyopathy using phosphoproteomics and a novel hiPSC-CM model.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: