Objective: To explore the role of platelet-derived growth factor-B (PDGF-B)/platelet-derived growth factor receptor-β (PDGFR-β) signaling in chronic atrial fibrillation (AF).
Methods: Thirty-nine AF patients and 33 patients with sinus rhythm (SR) were enrolled. Twenty canines were randomized into 5 groups: control, sham and AF lasting 1, 2 or 4 weeks. The AF canine models were made by rapid atrial pacing. Rat atrial fibroblasts were treated with PDGF-BB or PDGF-BB + PDGFR inhibitor AG1295, respectively. Gene expression in the right atrial appendage of patients, the left atrium of canines and rat atrial fibroblasts was measured by quantitative real-time PCR and Western blot, respectively. The degree of atrial fibrosis was evaluated by Masson trichrome staining.
Results: The degree of atrial fibrosis and the expression of PDGF-B, PDGFR-β and collagen type I (COL1) in AF patients significantly increased compared to patients with SR. The degree of atrial fibrosis and the expression of PDGF-B and COL1 in canines increased progressively with the increased duration of AF. The expression of PDGFR-β increased progressively 2 weeks after AF. PDGF-BB promoted the proliferation and COL1 secretion of rat atrial fibroblasts. AG1295 attenuated these effects.
Conclusions: Our study suggests that PDGF-B/PDGFR-β signaling, which promotes the proliferation and COL1 secretion of atrial fibroblasts, is an important contributor to atrial fibrosis in AF and may represent a novel target for the intervention of AF.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1159/000442940 | DOI Listing |
Nutrients
December 2024
Department of Food and Nutrition, Obesity/Diabetes Research Center, Hoseo University, 20 Hoseoro97bungil, BaeBang-Yup, Asan 31499, Republic of Korea.
Background: Myocardial infarction (MI) can range from mild to severe cardiovascular events and typically develops through complex interactions between genetic and lifestyle factors.
Objectives: We aimed to understand the genetic predisposition associated with MI through genetic correlation, colocalization analysis, and cells' gene expression values to develop more effective prevention and treatment strategies to reduce its burden.
Methods: A polygenic risk score (PRS) was employed to estimate the genetic risk for MI and to analyze the dietary interactions with PRS that affect MI risk in adults over 45 years ( = 58,701).
Mol Med
December 2024
Guang'anmen Hospital, Chinese Academy of Chinese Medical Sciences, No.5 Beixian'ge Street, Xicheng District, Beijing, 100053, China.
Aims: Atrial fibrillation (AF) has high mortality and morbidity rates. However, the intracellular molecular complexity of the atrial tissue of patients with AF has not been adequately assessed.
Methods And Results: We investigated the cellular heterogeneity of human atrial tissue and changes in differentially expressed genes between cells using single-cell RNA sequencing, fluorescence in situ hybridization, intercellular communication, and cell trajectory analysis.
Aims: Sacubitril/valsartan (Sac/Val) is used for treatment of heart failure. The effect of Sac/Val on regional dysfunction following myocardial infarction (MI) remains uncertain. This study aimed at understanding the effects of Sac/Val on regional function after MI.
View Article and Find Full Text PDFCells
November 2024
Division of Cardiology, Department of Internal Medicine, Shin Kong Wu Ho-Su Memorial Hospital, Taipei 11101, Taiwan.
Background: Atrial fibrillation (AF) is a common cardiac arrhythmia associated with significant morbidity and mortality. Rapid electrical stimulation (RES) of atrial fibroblasts plays a crucial role in AF pathogenesis, but the underlying molecular mechanisms remain unclear. This study investigates the regulatory axis involving MALAT1, miR-499a-5p, and SOX6 in human cardiac fibroblasts from adult atria (HCF-aa) under RES conditions.
View Article and Find Full Text PDFArch Med Sci
July 2024
Department of Laboratory Medicine, West China Hospital, Sichuan University, Chengdu, China.
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.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!