ArticleArchives of medical science : AMS2024
PPAR-α regulates metabolic remodelling and participates in myocardial fibrosis in patients with atrial fibrillation of rheumatic heart disease.
Article in Archives of medical science : AMS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Role of macrophage ATP metabolism disorder in SiOPurinergic signalling · 2025Review
- IL-11 promotes Ang II-induced autophagy inhibition and mitochondrial dysfunction in atrial fibroblasts.Open life sciences · 2025Article
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Authors and funding
4 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Introduction: This study will explore the correlation of peroxisome proliferator activated receptor-α (PPAR-α) regulation of metabolic remodelling in the myocardial fibrosis of atrial fibrillation (AF) in rheumatic heart disease. Material and methods: The left atrial appendage tissues were evaluated by Masson staining for fibrosis degree, and Western Blot was used to detect the expression of proteins related to glucose metabolism disorder, lipid metabolism abnormality, and mitochondrial dysfunction. The myocardial fibroblasts were established by stimulation with ANG II, and the PPAR-α agonist GW7647 was administered. The changes of phenotype transformation of myocardial fibroblasts were detected by cellular immunofluorescence, the secretion level of supernatant collagen was detected by ELISA. Finally, the correlation between PPAR-α protein expression and myocardial fibrosis was analysed and a conclusion was drawn. Results: Masson staining showed that the degree of myocardial fibrosis in patients with AF was significantly increased; WB analysis showed that there were statistically significant differences in protein expression related to glucose metabolism disorder, lipid metabolism abnormality, and mitochondrial dysfunction. There was a correlation between PPAR-α protein expression and myocardial fibrosis ( Conclusions: This study found that there is a negative correlation between the expression of PPAR-α protein and myocardial fibrosis in rheumatic heart disease AF, which plays a protective role. PPAR-α may participate in the pathogenesis of myocardial fibrosis in rheumatic heart disease AF by regulating glucose metabolism, lipid metabolism, and mitochondrial function.
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