Alternative splicing of TPM1 appears to be a previously underrecognized myofilament mechanism contributing to impaired relaxation and increased stiffness in heart failure with preserved ejection fraction (HFpEF).
The study identifies a specific pathogenic isoform shift toward TPM1b, generated by skipping exon 9a, in both human HFpEF samples and mouse models.
MedXY registered readers
Sign in free to continue reading
Create or use your MedXY account to unlock the complete article.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
