miR-29b ameliorates atrial fibrosis in rats with atrial fibrillation by targeting TGFβRΙ and inhibiting the activation of Smad-2/3 pathway

Han, Xinyuan; Wang, Shunda; Yong, Zhijun; Zhang, Xueting; Wang, Xuanqi

doi:10.1007/s10863-022-09934-7

Cited by 15 publications

(13 citation statements)

References 52 publications

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“…Thus, leveraging the concept of endothelial cell paracrine secretion could help to explore the mechanisms of lung fibrosis more effectively. In addition, SOX6 can also reverse renal fibrosis and cardiac fibrosis[35, 36]. LPS also promotes apoptosis in cardiomyocytes[37], especially upregulating SOX6, but lung fibrosis has not been studied.…”

Section: Discussionmentioning

confidence: 99%

Regulation of Interstitial Lung Diseases by Pulmonary Endothelial Cells via PLVAP

Zhang,

Jia,

Hou

et al. 2024

Preprint

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The lack of standardized treatments for Idiopathic Pulmonary Fibrosis (IPF) and non-IPF progressive fibrotic interstitial lung diseases (non-IPF-PF) highlights the need for identifying common therapeutic targets. We utilize single-cell RNA sequencing data from six disease groups, including IPF and non-IPF-PF such as Sarcoidosis, Systemic Sclerosis (SSc), Non-Specific Interstitial Pneumonitis (NSIP), myositis, and chronic eosinophilic pneumonia (cHP), we conducted subpopulation analysis to identify cells exhibiting a trend of upregulated expression. Pulmonary venous endothelial cells (PVECs) were identified as a significant subpopulation, and targets regulating PVECs upregulation were discerned. In addition, molecular targets are validated through the utilization of in vivo and in vitro methodologies. PVECs showed upregulation in IPF and non-IPF-PF, linked to poorer lung function. PLVAP was consistently elevated across both conditions. In vivo PLVAP knockdown in endothelial cells mitigated pulmonary fibrosis in a bleomycin mouse model, also reducing mesenchymal macrophage interactions. Our findings reveal common therapeutic targets in IPF and non-IPF-PF, offering new directions for treatment strategies.

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Section: Discussionmentioning

confidence: 99%

Regulation of Interstitial Lung Diseases by Pulmonary Endothelial Cells via PLVAP

Zhang,

Jia,

Hou

et al. 2024

Preprint

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“… 29 Overexpression of miR-30c was shown to reduce TGF-β1-induced rat CF proliferation, differentiation, and migration, and prevent atrial fibrosis in rat abdominal aortic constriction model by targeting TGF-βRII. 30 Other studies also demonstrated that miR-21 targeted Smad7, 31 miR-29b targeted TGF-βRI, 32 miR-135b targeted TGF-βRI, TGFβ-RII, and Smad2, 33 and miR-23b-3p and miR-27b-3p targeted two different sites in 3'-UTR of TGF-βRIII to participate in atrial fibrosis ( Table 1 ). 34 Additionally, miRNAs have been observed to target molecules linked with TGF-β1 signalling pathway, such as hsa-miR-4443 targeted THBS1, 35 miRNA-1202 targeted nNOS, 36 and miR-21 regulated WW domain-containing protein 1 ( Table 1 ).…”

Section: Mirnas and Arrhythmiasmentioning

confidence: 98%

Non-coding RNA and arrhythmias: expression, function, and molecular mechanism

Zeng

Zhang

et al. 2023

EP Europace

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Arrhythmias are a class of cardiac dysfunction characterized by heart rate disturbances and heart rhythm abnormalities, which are associated with substantial morbidity and mortality. Due to the limited understanding of pathological mechanism, current antiarrhythmic drugs and invasive therapies on arrhythmias lack sufficient efficacy and are always accompanied by potential adverse effects. Non-coding RNAs (including microRNAs, long non-coding RNAs, circular RNAs, and other small non-coding RNAs) have been demonstrated to be involved in the occurrence and development of various diseases including arrhythmias, which opens a new prospect for exploring the mechanism of arrhythmias and developing new therapeutic targets. Therefore, in this review, we aimed to provide an overview of the expression of ncRNAs in various arrhythmias, their roles in the arrhythmia’s development and pathophysiology, and the potential mechanism of ncRNAs in arrhythmias. As atrial fibrillation (AF) is the most common arrhythmia in clinical practice and current studies mainly focus on it, this review primarily discussed about AF. It was expected that this review may provide a basis for a better understanding of the mechanistic role of ncRNAs in arrhythmias and facilitate the development of mechanic-based therapeutic targets.

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“…The miR-29b is lowly expressed in AF rat atrial tissues. By promoting its expression, atrial fibrosis and AF in rats can be attenuated, which may be related to miR-29b by targeting TGFβRI and inhibiting the activation of the Smad2/3 signaling pathway ( Han et al, 2022 ). Furthermore, miR-135b is lowly expressed in AF patients, isoproterenol (ISO)-induced rat models, and in vitro rat cardiac fibroblasts (RCFs).…”

Section: Regulation Of Tgf-β/smad Signaling Pathway By Ncrnas In Card...mentioning

confidence: 99%

Mechanism of action of non-coding RNAs and traditional Chinese medicine in myocardial fibrosis: Focus on the TGF-β/Smad signaling pathway

Meng²,

Wang³

et al. 2023

Front. Pharmacol.

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Cardiac fibrosis is a serious public health problem worldwide that is closely linked to progression of many cardiovascular diseases (CVDs) and adversely affects both the disease process and clinical prognosis. Numerous studies have shown that the TGF-β/Smad signaling pathway plays a key role in the progression of cardiac fibrosis. Therefore, targeted inhibition of the TGF-β/Smad signaling pathway may be a therapeutic measure for cardiac fibrosis. Currently, as the investigation on non-coding RNAs (ncRNAs) move forward, a variety of ncRNAs targeting TGF-β and its downstream Smad proteins have attracted high attention. Besides, Traditional Chinese Medicine (TCM) has been widely used in treating the cardiac fibrosis. As more and more molecular mechanisms of natural products, herbal formulas, and proprietary Chinese medicines are revealed, TCM has been proven to act on cardiac fibrosis by modulating multiple targets and signaling pathways, especially the TGF-β/Smad. Therefore, this work summarizes the roles of TGF-β/Smad classical and non-classical signaling pathways in the cardiac fibrosis, and discusses the recent research advances in ncRNAs targeting the TGF-β/Smad signaling pathway and TCM against cardiac fibrosis. It is hoped, in this way, to give new insights into the prevention and treatment of cardiac fibrosis.

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miR-29b ameliorates atrial fibrosis in rats with atrial fibrillation by targeting TGFβRΙ and inhibiting the activation of Smad-2/3 pathway

Cited by 15 publications

References 52 publications

Regulation of Interstitial Lung Diseases by Pulmonary Endothelial Cells via PLVAP

Regulation of Interstitial Lung Diseases by Pulmonary Endothelial Cells via PLVAP

Non-coding RNA and arrhythmias: expression, function, and molecular mechanism

Mechanism of action of non-coding RNAs and traditional Chinese medicine in myocardial fibrosis: Focus on the TGF-β/Smad signaling pathway

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