Cardiac metabolic remodeling drives dicarbonyl stress-induced mitochondrial dysfunction in experimental heart failure with preserved ejection fraction

American Journal of Physiology-Heart and Circulatory Physiology 2026 Open access

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Authors: Ankit Aryal, Parnia Mobasheran, Luther Bishop, Sabyasachi Chatterjee, Scott Jennings, Huijing Xia, Eric Lazartigues, Qinglin Yang
DOI: 10.1152/ajpheart.00029.2026
Cited by: 3
References: 59

Abstract

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.

Fields of Study & Subjects

Cardiovascular Function and Risk Factors Mitochondrial Function and Pathology Cardiac Fibrosis and Remodeling

Publication details

Journal / source
American Journal of Physiology-Heart and Circulatory Physiology
Publisher
American Physiological Society
Volume
330
Issue
5
Pages
H1689–H1701
Publication date
21 April 2026
Language
EN