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Effect of Sox9 on TGF- β1-mediated atrial fibrosis
In conclusion, Sox9 is involved in the regulation of fibrosis in the atria and may be located downstream of TGF-β1. Our findings may provide a new perspective to treat atrial fibrosis during AF.PMID:34596216 | DOI:10.1093/abbs/gmab132
Source: Acta Biochimica et Biophysica Sinica - October 1, 2021 Category: Biochemistry Authors: Hechuan Wang Yiqi Chen Shuting Zhao Xiaowen Wang Kai Lu Hua Xiao Source Type: research

Pioglitazone Inhibits Diabetes-Induced Atrial Mitochondrial Oxidative Stress and Improves Mitochondrial Biogenesis, Dynamics, and Function Through the PPAR- γ/PGC-1α Signaling Pathway
Conclusion: Diabetes mellitus induces adverse atrial structural, electrophysiological remodeling, and mitochondrial damage and dysfunction. Pioglitazone prevented these abnormalities through the PPAR-γ/PGC-1α pathway.
Source: Frontiers in Pharmacology - June 14, 2021 Category: Drugs & Pharmacology Source Type: research

Crosstalk between the activated Slit2 –Robo1 pathway and TGF‐β1 signalling promotes cardiac fibrosis
ConclusionsThe Slit2 –Robo1 signalling pathway interfered with the TGF‐β1/Smad pathway and promoted cardiac fibrosis. Blockade of Slit2–Robo1 might be a new treatment for cardiac fibrosis.
Source: ESC Heart Failure - January 25, 2021 Category: Cardiology Authors: Yunqi Liu, Ziwei Yin, Xueqin Xu, Chen Liu, Xiaoying Duan, Qinlan Song, Ying Tuo, Cuiping Wang, Jing Yang, Shengli Yin Tags: Original Research Article Source Type: research

MFGE8 is down-regulated in cardiac fibrosis and attenuates endothelial-mesenchymal transition through Smad2/3-Snail signalling pathway.
In conclusion, our experiments indicate that MFGE8 might play a protective role in TGF-β1-induced EndMT and might be a potential therapeutic target for cardiac fibrosis. PMID: 32945126 [PubMed - as supplied by publisher]
Source: J Cell Mol Med - September 16, 2020 Category: Molecular Biology Authors: Wang B, Ge Z, Wu Y, Zha Y, Zhang X, Yan Y, Xie Y Tags: J Cell Mol Med Source Type: research

CYP2J2/EET reduces vulnerability to atrial fibrillation in chronic pressure overload mice.
In conclusion, this study revealed that CYP2J2/EET ameliorates atrial fibrosis through modulating atrial fibroblasts activation by disinhibition of MiR-21 on Smad-7, and attenuates atrial inflammatory response by repressing NF-κB pathways, reducing the vulnerability to AF, and CYP2J2/EET exerts its role at least partially through PPAR-γ activation. Our findings might provide a novel upstream therapeutic strategy for AF. PMID: 31749335 [PubMed - as supplied by publisher]
Source: J Cell Mol Med - November 19, 2019 Category: Molecular Biology Authors: Li X, Zhu F, Meng W, Zhang F, Hong J, Zhang G, Wang F Tags: J Cell Mol Med Source Type: research

An Inhibitor of Activated Blood Coagulation Factor X Shows Anti-Endothelial Senescence and Anti-Atherosclerotic Effects
Conclusion: Rivaroxaban prevents replicative senescence in HUVECs and aortic endothelial cells in dyslipidemic diabetic mice. It restores endothelial function and prevents the progression of atherosclerosis.J Vasc Res
Source: Journal of Vascular Research - July 2, 2019 Category: Research Source Type: research

Genetic Regulation of Liver Metabolites and Transcripts Linking to Biochemical-Clinical Parameters
Conclusion In summary, this study is the first to combine metabolomics, transcriptomics, and genome-wide association studies in a porcine model. Our results improve understanding of the genetic regulation of metabolites which link to transcripts and finally biochemical-clinical parameters. Further, high-performance profiling of metabolites as intermediate phenotypes is a potentially powerful approach to uncover how genetic variation affects metabolic and health status. Our results advance knowledge in areas of biomedical and agricultural interest and identify potential correlates of biomarkers, SNPs-metabolites, SNPs-tran...
Source: Frontiers in Genetics - April 16, 2019 Category: Genetics & Stem Cells Source Type: research

F-box protein-32 down-regulates small-conductance calcium-activated potassium channel 2 in diabetic mouse atria Molecular Bases of Disease
In conclusion, DM-induced SK2 channel down-regulation appears to be due to an FBXO-32-dependent increase in UPS-mediated SK2 protein degradation.
Source: Journal of Biological Chemistry - March 14, 2019 Category: Chemistry Authors: Tian-You Ling, Fu Yi, Tong Lu, Xiao-Li Wang, Xiaojing Sun, Monte S. Willis, Li-Qun Wu, Win-Kuang Shen, John P. Adelman, Hon-Chi Lee Tags: Molecular Bases of Disease Source Type: research

LIM kinase 1 acts as a profibrotic mediator in permanent atrial fibrillation patients with valvular heart disease.
Abstract Atrial fibrillation (AF) is the most frequently diagnosed cardiac arrhythmia worldwide. Patients with permanent atrial fibrillation are at an increased risk of developing valvular heart disease. Atrial fibrosis occurs in this pathophysiological setting. LIM kinase 1 (LIMK1) is a serine/threonine kinase that regulates microtubule stability and actin polymerization in fibroblasts. LIMK1 has been implicated in the pathogenesis of atrial fibrillation. Clinical data and biopsies of the right atrial appendage were collected from 50 patients with valvular heart disease who underwent heart valve replacement surge...
Source: Journal of Biosciences - February 28, 2019 Category: Biomedical Science Authors: Chen Q, Gimple RC, Li G, Chen J, Wu H, Li R, Xie J, Xu B Tags: J Biosci Source Type: research

Novel role of the clustered miR-23b-3p and miR-27b-3p in enhanced expression of fibrosis-associated genes by targeting TGFBR3 in atrial fibroblasts.
This study aimed to investigate the role of the clustered miR-23b-3p and miR-27b-3p in atrial fibrosis. Human atrial fibroblasts (HAFs) were isolated from atrial appendage tissue of patients with sinus rhythm. A cell model of atrial fibrosis was achieved in Ang-II-induced HAFs. Cell proliferation and migration were detected. We found that miR-23b-3p and miR-27b-3p were markedly increased in atrial appendage tissues of AF patients and in Ang-II-treated HAFs. Overexpression of miR-23b-3p and miR-27b-3p enhanced the expression of collagen, type I, alpha 1 (COL1A1), COL3A1 and ACTA2 in HAFs without significant effects on their...
Source: J Cell Mol Med - February 7, 2019 Category: Molecular Biology Authors: Yang Z, Xiao Z, Guo H, Fang X, Liang J, Zhu J, Yang J, Li H, Pan R, Yuan S, Dong W, Zheng XL, Wu S, Shan Z Tags: J Cell Mol Med Source Type: research

TWEAK/Fn14 mediates atrial-derived HL-1 myocytes hypertrophy via JAK2/STAT3 signalling pathway.
In conclusion, TWEAK/Fn14 axis mediates HL-1 atrial myocytes hypertrophy partly through activation of the JAK2/STAT3 pathway. PMID: 29971943 [PubMed - as supplied by publisher]
Source: J Cell Mol Med - July 4, 2018 Category: Molecular Biology Authors: Hao L, Ren M, Rong B, Xie F, Lin MJ, Zhao YC, Yue X, Han WQ, Zhong JQ Tags: J Cell Mol Med Source Type: research

Potential role of MG53 in the regulation of transforming-growth-factor- β1-induced atrial fibrosis and vulnerability to atrial fibrillation.
In conclusion, we demonstrated that MG53 was expressed in human atrium, and may be a potential upstream of the TGF-β1/Smad pathway in human atrium and rat atrial fibroblasts. This suggests that MG53 is a potential regulator of atrial fibrosis induced by the TGF-β1/Smad pathway in patients with AF. PMID: 29233682 [PubMed - as supplied by publisher]
Source: Experimental Cell Research - December 9, 2017 Category: Cytology Authors: Guo J, Jia F, Jiang Y, Li Q, Yang Y, Xiao M, Xiao H Tags: Exp Cell Res Source Type: research

Association between connexin 40 and potassium voltage-gated channel subfamily A member 5 expression in the atrial myocytes of patients with atrial fibrillation.
Authors: Zhang F, Bian Y, Huang L, Fan W Abstract Structural and electrical remodeling within the atrium mediate the pathogenesis of atrial fibrillation (AF). Two key genes that sever a role in this remodeling are connexin 40 (Cx40) and potassium voltage-gated channel subfamily A member 5 (KCNA5), respectively. Electrical remodeling is considered to induce structural remodeling during AF. In the present study, the left atrial appendage section and atrial myocytes of patients with AF were evaluated. It was observed that Cx40 and KCNA5 mRNA (P<0.05) and protein (P<0.01) expression was significantly downregulate...
Source: Experimental and Therapeutic Medicine - December 6, 2017 Category: General Medicine Tags: Exp Ther Med Source Type: research

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