PPAR-α regulates metabolic remodelling and participates in myocardial fibrosis in patients with atrial fibrillation of rheumatic heart disease
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...
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| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Termedia Publishing House
2024-07-01
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| Series: | Archives of Medical Science |
| Subjects: | |
| Online Access: | https://www.archivesofmedicalscience.com/PPAR-regulates-metabolic-remodelling-and-nparticipates-in-myocardial-fibrosis-in,181134,0,2.html |
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| Summary: | 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 ( r = –0.5322, p < 0.0001). After stimulation with
PPAR-α agonist GW7647, the phenotypic differentiation of myocardial fibro-
blasts into myofibroblasts was inhibited. The protein expression related
to mitochondrial dysfunction was statistically different.
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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| ISSN: | 1734-1922 1896-9151 |