ArticleJournal of advanced research2026
Peroxisomal dysfunction in cardiac adipose tissue is involved in obesity-associated cardiac hypertrophy.
Article in Journal of advanced research, 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
introductionCardiac adipose tissue, which directly interfaces with the myocardium and vasculature, has a pivotal role in obesity-related cardiovascular pathology through its metabolic activity. This tissue contributes to cardiac remodeling through its regulation of lipid metabolism. Among the key organelles involved, peroxisomes have a central role in lipid metabolism, yet their contribution to obesity-induced cardiac dysfunction remains poorly understood.
objectivesThis study investigated whether peroxisomal dysfunction in cardiac adipose tissue drives obesity-associated cardiac hypertrophy.
methodsUsing a high-fat diet (HFD)-induced obese rat model, we evaluated changes in cardiac adipose tissues, focusing on their browning capacity and metabolic functions. To investigate mechanistic effects, H9C2 cardiomyocytes were exposed either to fatty acids extracted from cardiac adipose tissues or conditioned medium derived from adipocytes treated with mitochondrial and peroxisomal inhibitors (Mdivi-1 or 10,12-tricosadiynoic acid).
resultsHFD-fed obese rats exhibited significant expansion of cardiac adipose tissues and cardiac hypertrophy, driven by impaired lipid metabolism and loss of browning capacity in cardiac fat associated with peroxisomal dysfunction. Treatment of H9C2 cardiomyocytes with conditioned medium from adipocytes with peroxisomal dysfunction induced collagen accumulation, increased expression of pro-inflammatory cytokines, and cellular hypertrophy, which recapitulates key pathological features observed in vivo.
conclusionOur findings demonstrate that peroxisomal dysfunction in cardiac adipose tissue drives lipid metabolic reprogramming and contributes to obesity-related cardiac hypertrophy. Targeting peroxisomal function in cardiac fat could be a novel therapeutic approach to mitigate obesity-induced cardiovascular remodeling.
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