Baicalin inhibits pressure overload-induced cardiac fibrosis through regulating AMPK/TGF-β/Smads signaling pathway

Xiao, Yichuan; Ye, Jiantao; Zhou, Ying; Huang, Junjun; Liu, Xiawen; Huang, Biyun; Zhu, Liu; Wu, Bo; Zhang, Gen-Shui; Cai, Yi

doi:10.1016/j.abb.2018.01.006

Cited by 61 publications

(38 citation statements)

References 37 publications

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“…Cao et al [106] studied cultured human vascular smooth muscle cells (hVSMCs), and discovered that the activation of AMPK by resveratrol inhibited AngII-induced phosphorylation of myosin phosphatase-targeting subunit 1 (MYPT1) and myosin light chain (MLC); Liraglutide, a GLP-1 receptor agonist, may inhibit VSMC proliferation which is induced by AngII. This is carried out by activating AMPK signaling and causing cell cycle arrest [107]; Baicalin prevented the development of cardiac fibrosis, mediated by AngII, by activating AMPK/TGF-β/Smads signaling pathway [108]; restoration of AMPK activity during AngII-induced hypertension ameliorates vascular function which was related to inhibition of NADPH-oxidase and xanthine oxidase activity. This result suggested AMPK as a possible pharmacological target in vascular disease [105]; AngII-induced human umbilical vein endothelial cells (HUVECs) senescence was improved by the apelin/APJ (one G protein-coupled receptor with seven transmembrane domains) axis via the AMPK-sirtuin 1 (SIRT1) signaling pathway, and the mechanisms might be associated with the suppressed production of ROS and the enhanced activity of telomerase [109].…”

Section: Angii and Ampk In Kidneymentioning

confidence: 99%

AMPK: a balancer of the renin–angiotensin system

Liu

et al. 2019

Bioscience Reports

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The renin–angiotensin system (RAS) is undisputedly well-studied as one of the oldest and most critical regulators for arterial blood pressure, fluid volume, as well as renal function. In recent studies, RAS has also been implicated in the development of obesity, diabetes, hyperlipidemia, and other diseases, and also involved in the regulation of several signaling pathways such as proliferation, apoptosis and autophagy, and insulin resistance. AMP-activated protein kinase (AMPK), an essential cellular energy sensor, has also been discovered to be involved in these diseases and cellular pathways. This would imply a connection between the RAS and AMPK. Therefore, this review serves to draw attention to the cross-talk between RAS and AMPK, then summering the most recent literature which highlights AMPK as a point of balance between physiological and pathological functions of the RAS.

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Section: Angii and Ampk In Kidneymentioning

confidence: 99%

AMPK: a balancer of the renin–angiotensin system

Liu

et al. 2019

Bioscience Reports

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“…11 Protein-protein interaction networks of BMPR-1B/FecB in ewe's ovary extracts based on GeneMANIA software of LH, the phosphorylated HSP 10 can close the gap junction between follicle and oocyte, which results in a decreased cAMP level in the oocyte. At the same time, calcium and calmodulin transfer the GnRH signal to the protein binding site of the tyrosine kinase receptor using the p38-MAPK pathway, which achieves the regulation of animal reproductive traits [32,33]. The results of Ling showed that HSP 10 was involved in the regulation of ovarian granulosa cell apoptosis, which might affect both the follicular and oocyte maturation.…”

Section: Discussionmentioning

confidence: 99%

Eukaryotic expression, Co-IP and MS identify BMPR-1B protein–protein interaction network

et al. 2020

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Background: BMPR-1B is part of the transforming growth factor β super family and plays a pivotal role in ewe litter size. Functional loss of exon-8 mutations in the BMPR-1B gene (namely the FecB gene) can increase both the ewe ovulation rate and litter size. Results: This study constructed a eukaryotic expression system, prepared a monoclonal antibody, and characterized BMPR-1B/FecB protein-protein interactions (PPIs). Using Co-immunoprecipitation coupled to mass spectrometry (Co-IP/MS), 23 proteins were identified that specifically interact with FecB in ovary extracts of ewes. Bioinformatics analysis of selected PPIs demonstrated that FecB associated with several other BMPs, primarily via signal transduction in the ovary. FecB and its associated interaction proteins enriched the reproduction process via BMP2 and BMP4 pathways. Signal transduction was identified via Smads proteins and TGF-beta signaling pathway by analyzing the biological processes and pathways. Moreover, other target proteins (GDF5, GDF9, RhoD, and HSP 10) that interact with FecB and that are related to ovulation and litter size in ewes were identified. Conclusions: In summary, this research identified a novel pathway and insight to explore the PPi network of BMPR-1B.

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“…This can be explained that curcumin abrogated the mesenchymal feature induced by TGF-β2 and restored the epithelial feature of LECs. Research showed that baicalin exerts antifibrosis effects via blocking the TGF-β/Smad signaling pathway [35]. Thus, the TGFβ/Smad signaling pathway is a potential target of alleviating pathogenic-fibrosis processes.…”

Section: Discussionmentioning

confidence: 99%

Curcumin Inhibits Proliferation and Epithelial-Mesenchymal Transition in Lens Epithelial Cells through Multiple Pathways

Liu

Mao

Xia

et al. 2020

BioMed Research International

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Background. Posterior capsule opacification (PCO), a complication of extracapsular lens extraction surgery that causes visual impairment, is characterized by aberrant proliferation and epithelial-mesenchymal transition (EMT) of lens epithelial cells (LECs). Curcumin, exerting inhibitive effects on cell proliferation and EMT in cancer, serves as a possible antidote towards PCO. Methods. Cellular proliferation of LECs after treatment of curcumin was measured with MTT assay and flow cytometry. The transcriptional and expressional levels of proteins related to proliferation and EMT of LECs were quantified by western blotting and real-time PCR. Results. Curcumin was found to suppress the proliferation of LECs by inducing G2/M arrest via possible inhibition of cell cycle-related proteins including CDK1, cyclin B1, and CDC25C. It had also inactivated proliferation pathways involving ERK1/2 and Akt pathways in LECs. On the other hand, curcumin downregulated the EMT of LECs through blocking the TGF-β/Smad pathway and interfering Notch pathway which play important roles in PCO. Conclusions. This study shows that curcumin could suppress the proliferation and EMT in LECs, and it might be a potential therapeutic protection against visual loss induced by PCO.

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Baicalin inhibits pressure overload-induced cardiac fibrosis through regulating AMPK/TGF-β/Smads signaling pathway

Cited by 61 publications

References 37 publications

AMPK: a balancer of the renin–angiotensin system

AMPK: a balancer of the renin–angiotensin system

Eukaryotic expression, Co-IP and MS identify BMPR-1B protein–protein interaction network

Curcumin Inhibits Proliferation and Epithelial-Mesenchymal Transition in Lens Epithelial Cells through Multiple Pathways

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