Astragaloside IV inhibits cardiac fibrosis via miR-135a-TRPM7-TGF-β/Smads pathway

Wei, Yanchun; Wu, Yan; Feng, Kai; Zhao, Yizhuo; Tao, Ran; Xu, Haonan; Tang, Yiqun

doi:10.1016/j.jep.2019.112404

Cited by 58 publications

(53 citation statements)

References 26 publications

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“…Evidence corroborates the existence of cross-regulation between the two ncRNAs mediated fibrosis-stimulating pathways and its role in cardiac fibrosis pathophysiology. Recognizing mechanisms associated with such cross-regulation provides possibilities for the development of new therapeutic approaches to reverse cardiac fibrosis (10)(11)(12). The present review examines TGF-β, as well as Smad signaling, followed by their contribution in the cardiac fibrosis pathogenesis.…”

Section: Introductionmentioning

confidence: 99%

“…It has been shown in mice that cardiac fibrosis related to pressure overload can be diminished by specific deletion of TGF-β1 or Smad3 gene in the triggered cardiac fibroblasts (CFs) (7). Non-coding RNAs (ncRNAs) include small microRNAs (miRNAs or miRs; > ∼22 nucleotides) and long non-coding RNAs (lncRNAs; > ∼200 nucleotides), as well as circular RNAs (circRNAs; > ∼200 circular nucleotides) (1), all of which are involved in regulating several signaling pathways, including TGF-β and Smad, for the control of cytokine release, along with ECM production (8)(9)(10). Evidence corroborates the existence of cross-regulation between the two ncRNAs mediated fibrosis-stimulating pathways and its role in cardiac fibrosis pathophysiology.…”

Section: Introductionmentioning

confidence: 99%

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Pivotal Role of TGF-β/Smad Signaling in Cardiac Fibrosis: Non-coding RNAs as Effectual Players

Saadat

Noureddini

Mahjoubin‐Tehran

et al. 2021

Front. Cardiovasc. Med.

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Unintended cardiac fibroblast proliferation in many pathophysiological heart conditions, known as cardiac fibrosis, results in pooling of extracellular matrix (ECM) proteins in the heart muscle. Transforming growth factor β (TGF-β) as a pivotal cytokine/growth factor stimulates fibroblasts and hastens ECM production in injured tissues. The TGF-β receptor is a heterodimeric receptor complex on the plasma membrane, made up from TGF-β type I, as well as type II receptors, giving rise to Smad2 and Smad3 transcription factors phosphorylation upon canonical signaling. Phosphorylated Smad2, Smad3, and cytoplasmic Smad4 intercommunicate to transfer the signal to the nucleus, culminating in provoked gene transcription. Additionally, TGF-β receptor complex activation starts up non-canonical signaling that lead to the mitogen-stimulated protein kinase cascade activation, inducing p38, JNK1/2 (c-Jun NH2-terminal kinase 1/2), and ERK1/2 (extracellular signal–regulated kinase 1/2) signaling. TGF-β not only activates fibroblasts and stimulates them to differentiate into myofibroblasts, which produce ECM proteins, but also promotes fibroblast proliferation. Non-coding RNAs (ncRNAs) are important regulators of numerous pathways along with cellular procedures. MicroRNAs and circular long ncRNAs, combined with long ncRNAs, are capable of affecting TGF-β/Smad signaling, leading to cardiac fibrosis. More comprehensive knowledge based on these processes may bring about new diagnostic and therapeutic approaches for different cardiac disorders.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Pivotal Role of TGF-β/Smad Signaling in Cardiac Fibrosis: Non-coding RNAs as Effectual Players

Saadat

Noureddini

Mahjoubin‐Tehran

et al. 2021

Front. Cardiovasc. Med.

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“…QSG is a Chinese prescription that enriches qi, promotes blood circulation, and removes water retention. A variety of Chinese herbs in QSG have been proven to have anti-heart failure effects [14][15][16][17].…”

Section: Discussionmentioning

confidence: 99%

Qishentaohong Granule as Adjuvant Therapy for Improving Cardiac Function and Quality of Life in Patients with Chronic Heart Failure: a Randomized Controlled Trial

Fan

Cui

et al. 2020

Preprint

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Background: Qishentaohong Granule (QSG) is a traditional Chinese medicine (TCM) prescription for the treatment of chronic heart failure (CHF). The objective is to confirm the improvement of QSG on cardiac function and quality of life (QOL) in patients with CHF.Methods: This is a single-center, prospective, randomized controlled clinical trial. Seventy-six patients (forty-four male and twenty-six female) from 27 to 84 years old with diagnosed CHF New York Heart Association (NYHA) classⅡ or Ⅲ in stage C were enrolled and randomly assigned in a 1:1 ratio to receive the QSG (9 g, twice daily) or trimetazidine (TMZ) (10 mg, thrice daily) in addition to their standard medications for the treatment of CHF. The study period was 4 weeks. The primary outcomes (cardiac function and QOL) and secondary outcomes were measured at the baseline and end of the trial.Results: Thirty-five patients completed the study in each group. At the 4-week follow-up, the efective rate in NYHA classification in the QSG group was better than that in the TMZ group (74.29% vs. 54.29%, P < 0.05). Chronic heart failure integrated traditional Chinese and Western medicine survival scale (CHFQLS) scores were improved by 13.82 ± 6.04 vs. 7.49 ± 2.28 in the QSG and TMZ groups respectively (P < 0.05). Subgroup analysis of the CHFQLS results showed that physiological function, role limitation and vitality were significantly higher in the QSG group (15.76 ± 7.85 vs. 7.40 ± 3.36, P < 0.05; 16.00 ± 8.35 vs. 10.53 ± 4.64, P < 0.05; 15.31 ± 8.09 vs. 7.89 ± 4.60, P < 0.05). Treatment with QSG also demonstrated superior performance in comparison to the TMZ with respect to 6-minute walking test (6MWT), TCM syndrome, shortness of breath, fatigue, gasp, general edema and the N-terminal pro-B-type natriuretic peptide (NT-proBNP) level. No significant adverse reactions (ARs) and adverse cardiac events (ACEs) occurred during treatment in either group.Conclusion: In addition to conventional treatments, QSG as an adjuvant therapy significantly improved cardiac function and QOL in patients with CHF class Ⅱ or Ⅲ in stage C.Trial registration: This trial is registered with ChiCTR, No. ChiCTR-TRC-12002857. Registered March 21, 2019. (retrospectively registered)

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“…Overexpression of miR-203 prevented cardiac collagen type I and type III expression in DCM mice by targeting PIK3CA through inactivation of the PI3K/Akt signaling pathway [ 131 ]. As upstream molecules of TGF-β, miR-135a, miR-122, miR-195, miR-202-3p, and miR-328 also participate in the process of fibrosis by regulating the expression of myocardial collagen [ 132 - 136 ]. Rubiś et al found that baseline serum levels of miR-21, miR-26, miR-29, and miR-30 were significantly different in DCM patients than in controls, and that MMP-2 levels were strongly associated with all of the microRNAs studied [ 137 ].…”

Section: Gene Transcription (Mirna)mentioning

confidence: 99%

Roles of Biomarkers in Myocardial Fibrosis

et al. 2020

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Myocardial fibrosis is observed in various cardiovascular diseases and plays a key role in the impairment of cardiac function. Endomyocardial biopsy, as the gold standard for the diagnosis of myocardial fibrosis, has limitations in terms of clinical application. Therefore, biomarkers have been recommended for noninvasive assessment of myocardial fibrosis. This review discusses the role of biomarkers in myocardial fibrosis from the perspective of collagen.

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Astragaloside IV inhibits cardiac fibrosis via miR-135a-TRPM7-TGF-β/Smads pathway

Cited by 58 publications

References 26 publications

Pivotal Role of TGF-β/Smad Signaling in Cardiac Fibrosis: Non-coding RNAs as Effectual Players

Pivotal Role of TGF-β/Smad Signaling in Cardiac Fibrosis: Non-coding RNAs as Effectual Players

Qishentaohong Granule as Adjuvant Therapy for Improving Cardiac Function and Quality of Life in Patients with Chronic Heart Failure: a Randomized Controlled Trial

Roles of Biomarkers in Myocardial Fibrosis

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