1,670 results match your criteria migration vsmcs


miR-141-5p suppresses vascular smooth muscle cell inflammation, proliferation, and migration via inhibiting the HMGB1/NF-κB pathway.

J Biochem Mol Toxicol 2021 Jun 14:e22828. Epub 2021 Jun 14.

Department of Pharmacy, Shanxi Cancer Hospital, Taiyuan, Shanxi, China.

MicroRNAs (miRNAs) have been identified as significant modulators in the pathogenesis of atherosclerosis (AS). Additionally, the dysregulation of vascular smooth muscle cells (VSMCs) is a crucial biological event during AS. Our study aimed to explore the functional roles and molecular mechanisms of miR-141-5p in VSMCs dysfunction. Read More

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The protective effect of HOXA5 on carotid atherosclerosis occurs by modulating the vascular smooth muscle cell phenotype.

Mol Cell Endocrinol 2021 Jun 11:111366. Epub 2021 Jun 11.

Department of Vascular Surgery, The First Hospital of China Medical University, Shenyang, China. Electronic address:

The phenotypic change of vascular smooth muscle cells (VSMCs) from a contractile to a synthetic form is a key player in atherogenic processes. Homeobox A5 (HOXA5), a transcription factor of the homeobox gene family, has been shown to regulate cell differentiation and morphogenesis. The present study was designed to clarify the involvement of HOXA5 in VSMC phenotypic transition in carotid atherosclerosis (CAS). Read More

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Inhibition of the Ras/ERK1/2 pathway contributes to the protective effect of ginsenoside Re against intimal hyperplasia.

Food Funct 2021 Jun 12. Epub 2021 Jun 12.

Department of Pharmacology, School of Basic Medical Sciences, Xi'an Jiaotong University, Xi'an, Shaanxi 710061, China.

Neointimal hyperplasia is the major cause of carotid stenosis after vascular injury, which restricts the long-term efficacy of endovascular treatment and endarterectomy in preventing stenosis. Ginsenoside Re (Re) is a major active ingredient of ginseng having multifaceted pharmacological effects on the cardiovascular system, and is a potential treatment for restenosis. In this study, we demonstrated that Re treatment significantly inhibited vascular injury-induced neointimal thickening, reduced the intimal area and intima/media (I/M) ratio, increased the lumen area, and inhibited pro-inflammatory cytokines. Read More

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MicroRNA-146b-3p regulates the dysfunction of vascular smooth muscle cells via repressing phosphoinositide-3 kinase catalytic subunit gamma.

Bioengineered 2021 Dec;12(1):2627-2638

Department of Cardiac Surgery, Dalian Municipal Center Hospital, Dalian Liaoning, China.

MicroRNAs are crucial regulators in the phenotype switch of vascular smooth muscle cells (VSMCs). Nonetheless, the role of miR-146b-3p in VSMCs remains unclear. In the present study, platelet-derived growth factor-BB (PDGF-BB) at different concentrations was employed to stimulate VSMCs for different times, to establish the model of VSMC dysfunction. Read More

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December 2021

miRNAs through β-ARR2/p-ERK1/2 pathway regulate the VSMC proliferation and migration.

Life Sci 2021 Jun 7;279:119703. Epub 2021 Jun 7.

Clinical Biochemistry Department, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran; Microbial Biotechnology Research Center, Iran University of Medical Sciences, Tehran, Iran. Electronic address:

Background: miRNAs are involved in plaque formation of atherosclerosis and vessel restenosis. In this study, we investigated the effects of miR-599, miR-204, and miR-181b on VSMC proliferation, and migration through TGFβ receptor 2 (TGFβR2), β-arrestin 2 (β-ARR2), SMAD2/p-SMAD2, and ERK1/2/p-ERK1/2.

Materials & Methods: Genes and miRNAs were predicted by bioinformatics tools and were transfected by PEI-miRNAs (miR-599, miR-204, and miR-181b) complexes into VSMCs. Read More

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miR-34c inhibits PDGF-BB-induced HAVSMCs phenotypic transformation and proliferation via PDGFR-β/SIRT1 pathway.

Mol Biol Rep 2021 Jun 10. Epub 2021 Jun 10.

Department of Neurosurgery, Affiliated Hospital of Southwest Medical University, 25 Taiping Road, Luzhou, 646000, Sichuan, People's Republic of China.

The purpose of this study was to explore the effect of miR-34c on PDGF-BB-induced HAVSMCs phenotypic transformation and proliferation via PDGFR-β/SIRT1 pathway, so as to find a new method for early diagnosis and treatment of cardiovascular disease. HA-VSMCs were treated with platelet-derived growth factor-BB (PDGF-BB) at 0 h, 12 h, 24 h, 48 h or 36 h to explore the optimal time for phenotypic transformation of VSMCs. And then, PDGF-BB-induced HA-VSMCs were transfected with miR-34c mimics/mimics NC and pcDNA3. Read More

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Micro-RNA-338-3p Promotes the Development of Atherosclerosis by Targeting Desmin and Promoting Proliferation.

Mol Biotechnol 2021 Jun 7. Epub 2021 Jun 7.

Department of Cardiology, Heze Municipal Hospital, No. 2888, Caozhou West Road, Heze, 274000, China.

Atherosclerosis (AS) is a dynamic and multi-stage process that involves various cells types, such as vascular smooth muscle cells (VSMCs) and molecules such as microRNAs. In this study, we investigated how miR-338-3p works in the process of AS. To determine how miR-338-3p was expressed in AS, an AS rat model was established and primary rat VSMCs were cultured. Read More

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SMYD3-PARP16 axis accelerates unfolded protein response and mediates neointima formation.

Acta Pharm Sin B 2021 May 15;11(5):1261-1273. Epub 2020 Dec 15.

Pharmacophenomics Laboratory, Human Phenome Institute, Fudan University, Shanghai 201203, China.

Neointimal hyperplasia after vascular injury is a representative complication of restenosis. Endoplasmic reticulum (ER) stress-induced unfolded protein response (UPR) is involved in the pathogenesis of vascular intimal hyperplasia. PARP16, a member of the poly(ADP-ribose) polymerases family, is correlated with the nuclear envelope and the ER. Read More

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MicroRNA-125b inhibits the proliferation of vascular smooth muscle cells induced by platelet-derived growth factor BB.

Exp Ther Med 2021 Aug 24;22(2):791. Epub 2021 May 24.

Department of Vascular Surgery, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233000, P.R. China.

Excessive proliferation and migration of vascular smooth muscle cells (VSMCs) is the main cause of arteriosclerosis obliterans (ASO). The present study aimed to investigate the role of microRNA (miR)-125b on the proliferation and migration of VSMCs. Platelet-derived growth factor-BB (PDGF-BB; 20 ng/ml) was used to treat VSMCs to establish an model of ASO. Read More

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Molecular Action of Hydroxytyrosol in Attenuation of Intimal Hyperplasia: A Scoping Review.

Front Pharmacol 2021 21;12:663266. Epub 2021 May 21.

Centre for Tissue Engineering and Regenerative Medicine, Universiti Kebangsaan Malaysia Medical Centre, Kuala Lumpur, Malaysia.

Hydroxytyrosol (HT), a polyphenol of olive plant is well known for its antioxidant, anti-inflammatory and anti-atherogenic properties. The aim of this systematic search is to highlight the scientific evidence evaluating molecular efficiency of HT in halting the progression of intimal hyperplasia (IH), which is a clinical condition arises from endothelial inflammation. A systematic search was performed through PubMed, Web of Science and Scopus, based on pre-set keywords which are Hydroxytyrosol OR 3,4-dihydroxyphenylethanol, AND Intimal hyperplasia OR Neointimal hyperplasia OR Endothelial OR Smooth muscles. Read More

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Circular RNA circLMF1 regulates PDGF-BB-induced proliferation and migration of human aortic smooth muscle cells by regulating the miR-125a-3p/VEGFA or FGF1 axis.

Clin Hemorheol Microcirc 2021 Jun 1. Epub 2021 Jun 1.

Department of Cardiac Surgery, The Cardio-Cerebro Vascular Disease Specialist Hospital of Qinghai Province, Xining City, China.

Atherosclerosis is a major cause of cardiovascular disease, in which vascular smooth muscle cells (VSMCs) proliferation and migration play a vital role. Circular RNAs (circRNAs) have been reported to be correlated with the VSMCs function. Therefore, this study is designed to explore the role and mechanism of circRNA lipase maturation factor 1 (circLMF1) in Human aortic VSMCs (HASMCs). Read More

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Curcumin-mediated photodynamic therapy inhibits the phenotypic transformation, migration, and foaming of oxidized low-density lipoprotein-treated vascular smooth muscle cells by promoting autophagy.

J Cardiovasc Pharmacol 2021 Jun 2. Epub 2021 Jun 2.

Department of Rehabilitation Medicine, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. Department of Rehabilitation Medicine Center, West China Hospital, Sichuan University, Chengdu, Sichuan, China; Key Laboratory of Rehabilitation Medicine in Sichuan Province, Chengdu, Sichuan, China.

Abstract: Vascular smooth muscle cells (VSMCs) are becoming a hot spot and target of atherosclerosis research. This study aimed to observe the specific effects of curcumin (CUR)-mediated photodynamic therapy (CUR-PDT) on oxidized low-density lipoprotein (ox-LDL)-treated VSMCs and confirm whether these effects are mediated by autophagy. In this study, the MOVAS and A7r5 cell lines were used for parallel experiments. Read More

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Role of vascular smooth muscle cell phenotypic switching in plaque progression: A hybrid modeling study.

J Theor Biol 2021 Jun 1;526:110794. Epub 2021 Jun 1.

School of Biological Sciences and Medical Engineering, Southeast University, Nanjing 210096, China; School of Mechanical, Medical and Process Engineering, Queensland University of Technology, Brisbane, QLD 4001, Australia. Electronic address:

Growing genetic lineage mapping experiments have definitively shown a wide-ranging plasticity of vascular smooth muscle cells (VSMCs) in atherosclerotic plaque and suggested that VSMCs can modulate their phenotypes in response to plaque microenvironment. Here, a multiscale hybrid discrete-continuous (HDC) modeling system is established to investigate the complex role of VSMC phenotypic switching within atherosclerotic lesions. The cellular behaviors of VSMCs and macrophages, including proliferation, migration, phenotypic transformation and necrosis, are determined by cellular automata (CA) rules in discrete model. Read More

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Vascular Adventitial Fibroblasts-Derived FGF10 Promotes Vascular Smooth Muscle Cells Proliferation and Migration in vitro and the Neointima Formation in vivo.

J Inflamm Res 2021 25;14:2207-2223. Epub 2021 May 25.

Department of Cardiology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200092, People's Republic of China.

Background: Activation of vascular adventitial fibroblasts (VAFs) upon vascular injury contributes greatly to the medial vascular smooth muscle cells (VSMCs) proliferation, migration and the subsequent neointima formation. A number of factors including fibroblast growth factors (FGFs) have been shown to control VSMC growth, proliferation and phenotypic switching, suggesting that they may function as paracrine signals for VAFs to modulate VSMCs functions. However, little is known about the signaling molecule(s) and its mechanism of action. Read More

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Neutrophil Elastase Promotes Neointimal Hyperplasia by Targeting TLR4-NFкB Signalling.

Br J Pharmacol 2021 Jun 2. Epub 2021 Jun 2.

Department of Cardiology, and Institute for Developmental and Regenerative Cardiovascular Medicine, Xinhua Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, 200092, China.

Background And Purpose: Neointimal hyperplasia (NIH) is the fundamental cause for vascular diseases, and vascular smooth muscle cell (VSMC) dysregulation has been widely implicated in NIH. Neutrophil elastase (NE) has been suggested as potential therapeutic for multiple diseases. Here we investigated the role of NE in VSMC functions and injury-induced NIH, and further explored the therapeutic potential of targeting NE in NIH. Read More

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Inhibitory Effect of a Glutamine Antagonist on Proliferation and Migration of VSMCs via Simultaneous Attenuation of Glycolysis and Oxidative Phosphorylation.

Int J Mol Sci 2021 May 25;22(11). Epub 2021 May 25.

Department of Biomedical Science, Graduate School, Kyungpook National University, Daegu 41566, Korea.

Excessive proliferation and migration of vascular smooth muscle cells (VSMCs) contribute to the development of atherosclerosis and restenosis. Glycolysis and glutaminolysis are increased in rapidly proliferating VSMCs to support their increased energy requirements and biomass production. Thus, it is essential to develop new pharmacological tools that regulate metabolic reprogramming in VSMCs for treatment of atherosclerosis. Read More

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Ambient Particulate Matter Induces Vascular Smooth Muscle Cell Phenotypic Changes via NOX1/ROS/NF-κB Dependent and Independent Pathways: Protective Effects of Polyphenols.

Antioxidants (Basel) 2021 May 14;10(5). Epub 2021 May 14.

National Institute of Environmental Health Sciences, National Health Research Institutes, Zhunan 53053, Taiwan.

Epidemiological studies have demonstrated an association between ambient particulate matter (PM) exposure and vascular diseases. Here, we observed that treatment with ambient PM increased cell migration ability in vascular smooth muscle cells (VSMCs) and pulmonary arterial SMCs (PASMCs). These results suggest that VSMCs and PASMCs transitioned from a differentiated to a synthetic phenotype after PM exposure. Read More

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Alternative C3 Complement System: Lipids and Atherosclerosis.

Int J Mol Sci 2021 May 12;22(10). Epub 2021 May 12.

Cardiovascular Program-ICCC, Research Institute-Hospital Santa Creu i Sant Pau, IIB-Sant Pau, 08025 Barcelona, Spain.

Familial hypercholesterolemia (FH) is increasingly associated with inflammation, a phenotype that persists despite treatment with lipid lowering therapies. The alternative C3 complement system (C3), as a key inflammatory mediator, seems to be involved in the atherosclerotic process; however, the relationship between C3 and lipids during plaque progression remains unknown. The aim of the study was to investigate by a systems biology approach the role of C3 in relation to lipoprotein levels during atherosclerosis (AT) progression and to gain a better understanding on the effects of C3 products on the phenotype and function of human lipid-loaded vascular smooth muscle cells (VSMCs). Read More

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CircMAPK1 promotes the proliferation and migration of vascular smooth muscle cells through miR-22-3p/ methyl-CpG binding protein 2 axis.

Nutr Metab Cardiovasc Dis 2021 Apr 20. Epub 2021 Apr 20.

Department of Cardiology, Shengjing Hospital of China Medical University, Shenyang, Liaoning, 110004, PR China. Electronic address:

Background And Aims: Atherosclerosis is a chronic inflammatory disease. The proliferation and migration of vascular smooth muscle cells (VSMCs) contribute to intimal hyperplasia. CircRNAs are class of endogenous RNA and implicated in the various biological processes. Read More

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Yixintongmai Inhibits Proliferation and Migration and Promotes Apoptosis of Vascular Smooth Muscle Cells Cultured with High Glucose.

Evid Based Complement Alternat Med 2021 4;2021:6583086. Epub 2021 May 4.

Division of Cardiology, The First Affiliated Hospital, College of Clinical Medicine, Henan University of Science and Technology, Luoyang 471003, China.

Objective: This study was designed to evaluate the effects of yixintongmai on proliferation, migration, and apoptosis of vascular smooth muscle cells (VSMCs) cultured with high glucose.

Methods: VSMCs of the thoracic aorta from 5- to 8-week-old male Sprague-Dawley rats were cultured with normal (4.5 mM) or high (25 mM) glucose, respectively. Read More

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Smooth muscle cell-specific knockout of interferon gamma (IFN-γ) receptor attenuates intimal hyperplasia via STAT1-KLF4 activation.

Life Sci 2021 May 25:119651. Epub 2021 May 25.

State Key Laboratory of Natural Medicines, Department of Pharmacology, China Pharmaceutical University, Nanjing, China. Electronic address:

Background: Intimal hyperplasia is a main contributor to in-stent restenosis. Previous researches have shown that interferon-gamma (IFN-γ), a pleiotropic pro-inflammatory factor, plays a pathological role in intimal hyperplasia. However, the specific role and molecular mechanism of vascular smooth muscle cells (VSMCs)-derived IFN-γ receptor in intimal hyperplasia remains unknown. Read More

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MFG-E8 Regulates Vascular Smooth Muscle Cell Migration Through Dose-Dependent Mediation of Actin Polymerization.

J Am Heart Assoc 2021 Jun 27;10(11):e020870. Epub 2021 May 27.

Department of Anatomy College of Medicine Chang Gung University Taoyuan Taiwan.

Background Migration of vascular smooth muscle cells (VSMCs) is the main contributor to neointimal formation. The Arp2/3 (actin-related proteins 2 and 3) complex activates actin polymerization and is involved in lamellipodia formation during VSMC migration. Milk fat globule-epidermal growth factor 8 (MFG-E8) is a glycoprotein expressed in VSMCs. Read More

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Curcumin inhibits the proliferation and migration of vascular smooth muscle cells by targeting the chemerin / CMKLR1 / LCN2 axis.

Aging (Albany NY) 2021 05 24;13(10):13859-13875. Epub 2021 May 24.

Department of Cardiology, Shenzhen People's Hospital, Jinan University, Shenzhen 518000, Guangdong, China.

Atherosclerosis (AS) is a chronic progressive inflammatory disease and a leading cause of death worldwide. Being a novel adipokine, chemerin is reported to be positively correlated with the severity of AS, yet its underlying mechanisms in AS remains elusive. It is well-known that AS development is significantly attributed to abnormal proliferation and migration of vascular smooth muscle cells (VSMCs). Read More

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Long non-coding RNA MIAT regulates ox-LDL-induced cell proliferation, migration and invasion by miR-641/STIM1 axis in human vascular smooth muscle cells.

BMC Cardiovasc Disord 2021 May 20;21(1):248. Epub 2021 May 20.

Department of Cardiac Surgery, Central Hospital Affiliated to Shandong First Medical University, No.105, Jiefang Road, Jinan, 250013, Shandong, People's Republic of China.

Background: Atherosclerosis (AS) is a primary cause of coronary heart and vascular diseases. Long non-coding RNAs (lncRNAs) are indicated to regulate AS progression. This study aimed to reveal the biological roles of lncRNA myocardial infarction associated transcript (MIAT) in oxidized low-density lipoprotein (ox-LDL)-induced human vascular smooth muscle cells (VSMCs). Read More

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Redox-sensitive enzyme SENP3 mediates vascular remodeling via de-SUMOylation of β-catenin and regulation of its stability.

EBioMedicine 2021 May 14;67:103386. Epub 2021 May 14.

Heart Center, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai 200030, China. Electronic address:

Background: Oxidative stress plays critical pathophysiological roles in vascular remodeling-related cardiovascular diseases, including hypertension, atherosclerosis, and restenosis. Previous studies demonstrate that SENP3, a redox-sensitive SUMO2/3-specific protease, is strongly implicated in cancer development and progression. However, the role of SENP3 in vascular remodeling remains unknown. Read More

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Circ_CHFR promotes PDGF-BB-induced proliferation, invasion and migration in VSMCs via miR-149-5p/NRP2 axis.

J Cardiovasc Pharmacol 2021 May 10. Epub 2021 May 10.

Department of Cardiovascular Medicine, The First Affiliated Hospital of Xi'an Medical University, Xi'an, 710077, Shaanxi, China Department of General Practice, The First Affiliated Hospital of Xi'an Medical University, Xi'an, 710077, Shaanxi, China.

Abstract: Circular RNA Checkpoint With Forkhead And Ring Finger Domains (circ_CHFR) was reported to regulate vascular smooth muscle cell (VSMC) dysfunction during atherosclerosis (AS). However, the molecule mechanism of circ_CHFR in AS remains largely unclear. Human VSMCs (HVSMCs) were exposed to platelet-derived growth factor-bb (PDGF-BB) in vitro. Read More

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Deletion of inhibits neointima formation by enhancing KAT2A/GCN5-mediated acetylation of TUBA/α-tubulin .

Autophagy 2021 May 14:1-18. Epub 2021 May 14.

Center of Molecular and Translational Medicine, Georgia State University, Atlanta, Georgia.

ULK1 (unc-51 like autophagy activating kinase) has a central role in initiating macroautophagy/autophagy, a process that contributes to atherosclerosis and neointima hyperplasia, or excessive tissue growth that leads to vessel dysfunction. However, the role of ULK1 in neointima formation remains unclear. We aimed to determine how deletion affected neointima formation and to investigate the underlying mechanisms. Read More

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Blocking circ_UBR4 suppressed proliferation, migration, and cell cycle progression of human vascular smooth muscle cells in atherosclerosis.

Open Life Sci 2021 27;16(1):419-430. Epub 2021 Apr 27.

Department of Cardiology, Zhongshan Affiliated Hospital, Dalian University, No. 6, Zhonshan Road, Dalian, 116001, Liaoning, China.

The circ_UBR4 (hsa_circ_0010283) is a novel abnormally overexpressed circRNA in oxidized low-density lipoprotein (ox-LDL)-induced model of atherosclerosis (AS) in human vascular smooth muscle cells (VSMCs). However, its role in the dysfunction of VSMCs remains to be further investigated. Here, we attempted to explore its role in ox-LDL-induced excessive proliferation and migration in VSMCs by regulating Rho/Rho-associated coiled-coil containing kinase 1 (ROCK1), a therapeutic target of AS. Read More

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Effect of miR-126 on the Proliferation and Migration of Vascular Smooth Muscle Cells in Aortic Aneurysm Mice Under PI3K/AKT/mTOR Signaling Pathway.

Mol Biotechnol 2021 Jul 10;63(7):631-637. Epub 2021 May 10.

Department of Vascular Surgery, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, 310006, Zhejiang Province, China.

This paper is to investigate the expression changes of Phosphatidylinositol-3 Kinase (PI3K), protein kinase B (AKT), and Mammalian Target of Rapamycin (mTOR) in Vascular Smooth Muscle Cells (VSMCs) of aortic aneurysm mice, and to analyze the mechanism of VSMCs proliferation and migration. Aortic VSMCs cells were cultured using BALB/c mice as the research object. VSMCs were identified using artificial intelligence-based digital microscopy equipment, and liposome-transfected VSMCs experiments were performed. Read More

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Wnt Signaling Cascades and Their Role in Coronary Artery Health and Disease.

J Cell Signal 2021 ;2(1):52-62

Section of Cardiovascular Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06510, USA.

The Wnt signaling is classified as two distinct pathways of canonical Wnt/β-catenin signaling, and the non-canonical pathways of planar cell polarity and Wnt/Ca pathways. However, the scientific discoveries in recent years have shown that canonical and non-canonical Wnts pathways are intertwined and have complex interaction with other major signaling pathways such as hedgehog, Hippo and TOR signaling. Wnt signaling plays important roles in cell proliferation, differentiation and migration during embryonic development. Read More

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January 2021