ArticleMolecular and cellular biochemistry2026
Betulinic acid attenuates obesity-associated cardiac remodelling by modulating mitochondrial quality control, ferroptosis-associated signalling, and calcium-regulatory pathways.
Article in Molecular and cellular biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Obesity-associated cardiac remodelling (OACR) is characterized by metabolic, structural, mitochondrial, oxidative, and molecular alterations that may contribute to progressive cardiac dysfunction. However, the interplay among mitochondrial quality control, ferroptosis, and calcium homeostasis in obesity-associated cardiac injury and remodelling remains incompletely understood. This study investigated whether betulinic acid (BA) attenuates obesity-induced myocardial injury by modulating these interconnected pathways. Male Sprague-Dawley rats were fed a high-fat diet (HFD) for 16 weeks to induce cardiac injury and remodelling and treated with BA (40 mg/kg, orally) for 6 weeks. Cardiac morphology, metabolic parameters, myocardial bioenergetic parameters, oxidative stress, iron homeostasis, and markers associated with mitochondrial quality control, mitochondrial dynamics, ferroptosis, and calcium regulation were assessed using biochemical, histopathological, mRNA, and protein expression analyses. Molecular docking provided hypothesis-generating predictions of potential interactions between BA and selected regulatory proteins. HFD-induced obesity was associated with alterations in mitochondrial quality-control, ferroptosis-associated, and calcium-regulatory signalling markers, including changes in the SERCA2a-CaMKIIδ axis. BA improved metabolic abnormalities, increased myocardial ATP content and the NAD⁺/NADH ratio, and attenuated oxidative injury and iron accumulation. These effects were accompanied by increased PINK1, Parkin, MFN2, GPX4, SLC7A11, and SERCA2a expression and decreased DRP1, ACSL4, and CaMKIIδ expression. BA attenuated OACR, accompanied by changes in mitochondrial quality-control, ferroptosis-associated, and calcium-regulatory proteins. These findings indicate that modulation of these interconnected pathways may contribute to the attenuation of OACR.
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