Atrial fibrosis and atrial fibrillation: The role of the TGF-β1 signaling pathway

Gramley, Felix; Lorenzen, Johann; Koellensperger, Eva; Kettering, Klaus; Weiß, Christian; Münzel, Thomas

doi:10.1016/j.ijcard.2009.03.110

Cited by 103 publications

(75 citation statements)

References 47 publications

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“…Interestingly, a recent study showed that TGF-␤ inhibits adipogenesis and induces myogenesis simultaneously in a dose-dependent manner in progenitor cells obtained from the left atrium of adult rats (14). TGF-␤ signaling has also shown to be involved in atrial fibrosis in patients with atrial fibrillation (8), which further strengthens the notion of an important role for TGF-␤ signaling in the atrium. The basic helix-loop-helix transcription factor HEY2, on the other hand, with a known role in cardiac development, was found to be more highly expressed in LV.…”

Section: Discussionmentioning

confidence: 72%

Comparison of human cardiac gene expression profiles in paired samples of right atrium and left ventricle collected in vivo

Asp

Synnergren

Jönsson

et al. 2012

Physiological Genomics

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Section: Discussionmentioning

confidence: 72%

Comparison of human cardiac gene expression profiles in paired samples of right atrium and left ventricle collected in vivo

Asp

Synnergren

Jönsson

et al. 2012

Physiological Genomics

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“…This is an increasing responsiveness to increased TGF-β1. However, Gramley et al 23 found that human atrial fibrogenesis in patients with atrial fibrillation is accompanied by a biphasic response, an early increase and later loss of responsiveness to TGF-β1. Because of the small sample size (38 patients) and no full grouping of AF (3 groups), further detailed and extensive research to explore the mechanism of human atrial fibrosis should be done.…”

Section: Discussionmentioning

confidence: 99%

TGF‐β1 Expression and Atrial Myocardium Fibrosis Increase in Atrial Fibrillation Secondary to Rheumatic Heart Disease

Xiao

Shu

et al. 2010

Clinical Cardiology

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Background:Atrial fibrosis was considered a structural basis for the development and sustaining of atrial fibrillation (AF). Transforming growth factor‐β1 (TGF‐β1) was one of the main factors for accelerating collagen production. The contribution of TGF‐β1 in the pathogenesis of AF needs further investigation.Hypothesis:The altered expression and distribution of TGF‐β1 will be associated with the changes in atrial fibrosis in different types of AF patients with rheumatic heart disease (RHD).Methods:Right atrial specimens obtained from 38 RHD patients undergoing mitral valve replacement surgery were divided into 3 groups: the sinus rhythm group (n = 8), the paroxysmal AF group (pAF; n = 10), and the chronic AF group (cAF; AF lasting ≥ 6 mo; n = 20). The degree of atrial fibrosis, collagen content, serum levels, messenger RNA (mRNA), and protein expression of TGF‐β1 were detected.Results:The collagen content, serum level, TGF‐β1 mRNA, and protein expression of the atrial tissue increased gradually in sinus rhythm, for both pAF and cAF groups, respectively. A positive correlation between TGF‐β1 and the degree of atrial fibrosis was also demonstrated (P < 0.05).Conclusion:The TGF‐β1 expression in atrial tissue increased gradually in proportion to the degree of atrial fibrosis in AF and was associated with the type of AF, which suggests that TGF‐β1 is possibly involved in the pathogenesis of AF in RHD patients. Copyright © 2010 Wiley Periodicals, Inc.

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“…The link between ECM remodelling and AF maintenance is now universally recognized. As a result, atrial non‐homogeneity in conduction contributes to the maintenance and progression of AF 36, 37, 38. Our previous study clearly indicated that permanent ventricular pressure overload by AAC induces atrial remodelling, including hypertrophy, dilatation and fibrosis, and susceptibility to AF 39.…”

Section: Discussionmentioning

confidence: 98%

MicroRNA‐30c suppresses the pro‐fibrogenic effects of cardiac fibroblasts induced by TGF‐β1 and prevents atrial fibrosis by targeting TGFβRII

Wang

Chen

et al. 2018

J Cellular Molecular Medi

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Atrial fibrosis serves as an important contributor to atrial fibrillation (AF). Recent data have suggested that microRNA‐30c (miR‐30c) is involved in fibrotic remodelling and cancer development, but the specific role of miR‐30c in atrial fibrosis remains unclear. The purpose of this study was to investigate the role of miR‐30c in atrial fibrosis and its underlying mechanisms through in vivo and in vitro experiments. Our results indicate that miR‐30c is significantly down‐regulated in the rat abdominal aortic constriction (AAC) model and in the cellular model of fibrosis induced by transforming growth factor‐β1 (TGF‐β1). Overexpression of miR‐30c in cardiac fibroblasts (CFs) markedly inhibits CF proliferation, differentiation, migration and collagen production, whereas decrease in miR‐30c leads to the opposite results. Moreover, we identified TGFβRII as a target of miR‐30c. Finally, transferring adeno‐associated virus 9 (AAV9)‐miR‐30c into the inferior vena cava of rats attenuated fibrosis in the left atrium following AAC. These data indicate that miR‐30c attenuates atrial fibrosis via inhibition of CF proliferation, differentiation, migration and collagen production by targeting TGFβRII, suggesting that miR‐30c might be a novel potential therapeutic target for preventing atrial fibrosis.

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Atrial fibrosis and atrial fibrillation: The role of the TGF-β1 signaling pathway

Cited by 103 publications

References 47 publications

Comparison of human cardiac gene expression profiles in paired samples of right atrium and left ventricle collected in vivo

Comparison of human cardiac gene expression profiles in paired samples of right atrium and left ventricle collected in vivo

TGF‐β1 Expression and Atrial Myocardium Fibrosis Increase in Atrial Fibrillation Secondary to Rheumatic Heart Disease

MicroRNA‐30c suppresses the pro‐fibrogenic effects of cardiac fibroblasts induced by TGF‐β1 and prevents atrial fibrosis by targeting TGFβRII

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