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Targeting Inflammation by Pioglitazone and its R-Enantiomer Mitigates Pathological Myocardial Remodeling in Murine Hypertrophic Cardiomyopathy
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DOI：10.1016/j.jacbts.2026.101574.png)
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Abstract
En 中文
• Energetic, inflammatory, and metabolic dysregulation are key drivers of disease progression in HCM. • Targeted modulation of these pathways ameliorates hypertrophy and fibrosis in an HCM mouse model. • PPARγ-independent metabolic intervention of R-pio represents a promising strategy to counteract upstream drivers of HCM remodeling.
Keywords:
hypertrophic cardiomyopathy
inflammation and oxidative stress
mitochondrial dysfunction
myocardial hypertrophy and fibrosis
pioglitazone
HCM
hypertrophic cardiomyopathy
NULISA
Nucleic Acid Linked Immuno-Sandwich Assay
pio
pioglitazone
R-pio
R-enantiomer of pioglitazone
WT
wild-type
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