Changes in cardiac myosin acetylation disrupt the super-relaxed state in genotype-negative hypertrophic cardiomyopathy with type 2 diabetes.

doi:10.1186/s12933-026-03211-2

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Changes in cardiac myosin acetylation disrupt the super-relaxed state in genotype-negative hypertrophic cardiomyopathy with type 2 diabetes.

Cardiovascular diabetology - 26 May 2026

Nollet Edgar E, Chaami Chahida, Bogdanovic Keleman Helena, Gerlach Melhedegaard Elise, Lewis Christopher T A, Seaborne Robert A E, Visch Julia E, Schoonvelde Stephan A C, Feng Miao, Wang Qian, Hessel Anthony L, Kuehn Michel N, Schomakers Bauke V, van Weeghel Michel, Michels Michelle, Kuster Diederik W D, van der Velden Jolanda, Ochala Julien

Abstract excerpt

BACKGROUND: Patients with hypertrophic cardiomyopathy (HCM) and type 2 diabetes (T2D) have a more severe cardiac phenotype and worse clinical course than non‑diabetic patients. To identify how T2D aggravates the disease and whether the most abundant cardiac protein, myosin, is involved, we combined functional, structural and mass spectrometry analyses of human samples. METHODS: Left ventricular septal myectomy...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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PMID: 42192426
DOI: 10.1186/s12933-026-03211-2

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