Loss of SIRT2 in cardiomyocytes reduces glycolytic flux via increased acetylation of glycolytic enzymes

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

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Authors: Ezra B. Ketema, Ruth Han, Muhammad Ahsan, Fariha Fairuz, Kaya L. Persad, Qiuyu Sun, Liyan Zhang, Jason R.B. Dyck, Gary D. Lopaschuk
DOI: 10.1152/ajpheart.00145.2026
Cited by: 1
References: 46

Abstract

Protein lysine acetylation differentially regulates cardiac fatty acid and glucose oxidation. However, its role in controlling glycolysis remains poorly defined. Using pharmacological inhibition and siRNA-mediated knockdown of sirtuin 2 (SIRT2), we demonstrate that loss of SIRT2 increases acetylation of glycolytic enzymes and reduces cardiac glycolytic flux in isolated working hearts and cardiomyocytes, independent of insulin signaling. Our findings reveal an important role of SIRT2-dependent deacetylation in regulating cardiac glycolytic flux.

Fields of Study & Subjects

Sirtuins and Resveratrol in Medicine Endoplasmic Reticulum Stress and Disease Signaling Pathways in Disease

Publication details

Journal / source
American Journal of Physiology-Heart and Circulatory Physiology
Publisher
American Physiological Society
Volume
331
Issue
1
Pages
H202–H213
Publication date
1 June 2026
Language
EN