Cardiac metabolic remodeling drives dicarbonyl stress-induced mitochondrial dysfunction in experimental heart failure with preserved ejection fraction
Recent studies increasingly highlight profound metabolic remodeling within the HFpEF heart; however, it remains unclear if this is an intrinsic or systemic phenomenon. In the present study, we identify dicarbonyl and glycative stress as key drivers of mitochondrial dysfunction in an ANGII/PE mouse model with HFpEF phenotype independent of systemic metabolic disease. These findings reveal a previously unrecognized metabolic-mitochondrial axis and suggest dicarbonyl detoxification and mitochondrial antiglycation as potential therapeutic targets.
Authors
- Eric Lazartigues (ORCID: https://orcid.org/0000-0001-7290-0786)
- Ankit Aryal (ORCID: https://orcid.org/0000-0002-1691-5112)
- Qinglin Yang (ORCID: https://orcid.org/0000-0002-6024-2517)
- Huijing Xia (ORCID: https://orcid.org/0000-0001-7024-5693)
- Scott Jennings
- Parnia Mobasheran (ORCID: https://orcid.org/0009-0003-3582-1669)
- Sabyasachi Chatterjee
- Luther Bishop
Institutions
- Louisiana State University Health Sciences Center New Orleans (US)
Publication Details
- Journal
- American Journal of Physiology-Heart and Circulatory Physiology
- Published
- 2026-04-21
- DOI
- https://doi.org/10.1152/ajpheart.00029.2026
- Primary Topic
- Cardiovascular Function and Risk Factors
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- National Science Foundation
- National Heart, Lung, and Blood Institute