Cardiomyocyte Reduction of Hybrid/Complex N‐Glycosylation in the Adult Causes Heart Failure With Reduced Ejection Fraction in the Absence of Cellular Remodeling
The tamoxifen-inducible, cardiomyocyte <i>Mgat1</i> knockout mouse strain created and characterized here provides a model to describe novel mechanisms and causes responsible for HFrEF onset in the adult, likely occurring primarily through tissue-level reductions in electromechanical activity in the absence of (or at least before) cardiomyocyte remodeling and fibrosis.
Authors
- John A. Miller (ORCID: https://orcid.org/0009-0005-7770-1336)
- Eric S. Bennett (ORCID: https://orcid.org/0000-0002-1605-7250)
- Andrew R. Ednie (ORCID: https://orcid.org/0000-0002-6796-9516)
- Anthony Young (ORCID: https://orcid.org/0000-0002-4593-7396)
Institutions
- Wright State University (US)
Publication Details
- Journal
- Journal of the American Heart Association
- Published
- 2024-10-11
- DOI
- https://doi.org/10.1161/jaha.124.036626
- Citations
- 4
- Primary Topic
- Glycosylation and Glycoproteins Research
- Type
- article
- Field-Weighted Citation Impact
- 0.94
Funders
- National Science Foundation
- Division of Molecular and Cellular Biosciences