Destabilization of cardiac myosin acetylation and sequestration with type 2 diabetes mellitus
Human T2DM myocardium exhibits early, site‑specific myosin acetylations that destabilize myosin structural OFF‑state. This myosin 'preload' remodeling occurs at no energetic cost and may constitute a potential early marker of latent myocardial vulnerability in T2DM.
Authors
- Robert A. Seaborne (ORCID: https://orcid.org/0000-0003-2491-3747)
- Mathis K. Stokke (ORCID: https://orcid.org/0000-0002-8869-8153)
- Julien Ochala (ORCID: https://orcid.org/0000-0002-6358-2920)
- Chengxin Zhang (ORCID: https://orcid.org/0000-0002-1771-8313)
- Anthony L. Hessel (ORCID: https://orcid.org/0000-0003-4278-4221)
- P. Rainer
- Chahida Chaami (ORCID: https://orcid.org/0009-0007-2597-1566)
- Mahault Mathilde Degezelle
- Christopher T. A. Lewis
- Jonathan A. Kirk
Institutions
- University of Copenhagen (DK)
- Oslo University Hospital (NO)
- King's College London (GB)
- University of Oslo (NO)
- Loyola University Chicago (US)
- Medical University of Graz (AT)
- University of Michigan (US)
- Tyrolit (Austria) (AT)
- BioTechMed-Graz (AT)
- Institutt for Eksperimentell Medisinsk Forskning (NO)
- Ophthalmic Consultants of Boston (US)
- Spanish National Centre for Cardiovascular Research (ES)
Publication Details
- Journal
- Cardiovascular Diabetology
- Published
- 2026-01-16
- DOI
- https://doi.org/10.1186/s12933-025-03052-5
- Primary Topic
- Cardiac Structural Anomalies and Repair
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- U.S. Department of Energy
- Novo Nordisk
- Novo Nordisk Fonden
- Simon Fougner Hartmanns Familiefond
- National Institutes of Health
- Office of Science
- National Institute of General Medical Sciences
- Biological and Environmental Research
- Brookhaven National Laboratory