3,044 results match your criteria human 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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TET2 Protects Against VSMC Apoptosis and Intimal Thickening in Transplant Vasculopathy.

Circulation 2021 Jun 11. Epub 2021 Jun 11.

Department of Medicine (Cardiovascular Medicine), Yale University School of Medicine, New Haven, CT.

Coronary allograft vasculopathy (CAV) is a devastating sequelae of heart transplant in which arterial intimal thickening limits coronary blood flow. There are currently no targeted therapies to prevent or reduce this pathology that leads to transplant failure. Vascular smooth muscle cell (VSMC) phenotypic plasticity is critical in CAV neointima formation. Read More

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Inhibition of CDK9 attenuates atherosclerosis by inhibiting inflammation and phenotypic switching of vascular smooth muscle cells.

Aging (Albany NY) 2021 Jun 8;13(undefined). Epub 2021 Jun 8.

Chemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325035, China.

Background: Recent studies have demonstrated a key role of vascular smooth muscle cell (VSMC) dysfunction in atherosclerosis. Cyclin-dependent kinases 9 (CDK9), a potential biomarker of atherosclerosis, was significantly increased in coronary artery disease patient serum and played an important role in inflammatory diseases. This study was to explore the pharmacological role of CDK9 inhibition in attenuating atherosclerosis. 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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Positive Association of Leptin and Artery Calcification of Lower Extremity in Patients With Type 2 Diabetes Mellitus: A Pilot Study.

Front Endocrinol (Lausanne) 2021 19;12:583575. Epub 2021 May 19.

Laboratory of Cardiovascular Bioactive Molecule, School of Basic Medical Sciences, Peking University, Beijing, China.

Objective: We aimed to explore the role and possible mechanism of leptin in lower-extremity artery calcification in patients with type 2 diabetes mellitus (T2DM).

Methods: We recruited 59 male patients with T2DM and 39 non-diabetic male participants. All participants underwent computed tomography scan of lower-extremity arteries. 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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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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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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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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Fate and State of Vascular Smooth Muscle Cells in Atherosclerosis.

Circulation 2021 May 24;143(21):2110-2116. Epub 2021 May 24.

Center for Developmental Biology and Regenerative Medicine, Department of Pediatrics, University of Washington, Seattle Children's Research Institute (M.W.M.).

Vascular smooth muscle cells (VSMCs) have long been associated with phenotypic modulation/plasticity or dedifferentiation. Innovative technologies in cell lineage tracing, single-cell RNA sequencing, and human genomics have been integrated to gain unprecedented insights into the molecular reprogramming of VSMCs to other cell phenotypes in experimental and clinical atherosclerosis. The current thinking is that an apparently small subset of contractile VSMCs undergoes a fate switch to transitional, multipotential cells that can adopt plaque-destabilizing (inflammation, ossification) or plaque-stabilizing (collagen matrix deposition) cell states. Read More

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Telomere damage promotes vascular smooth muscle cell senescence and immune cell recruitment after vessel injury.

Commun Biol 2021 May 21;4(1):611. Epub 2021 May 21.

Division of Cardiovascular Medicine, University of Cambridge, Addenbrooke's Centre for Clinical Investigation, Addenbrooke's Hospital, Cambridge, UK.

Accumulation of vascular smooth muscle cells (VSMCs) is a hallmark of multiple vascular pathologies, including following neointimal formation after injury and atherosclerosis. However, human VSMCs in advanced atherosclerotic lesions show reduced cell proliferation, extensive and persistent DNA damage, and features of premature cell senescence. Here, we report that stress-induced premature senescence (SIPS) and stable expression of a telomeric repeat-binding factor 2 protein mutant (TRF2) induce senescence of human VSMCs, associated with persistent telomeric DNA damage. 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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Single-Cell Transcriptome Analysis of Human Adipose-Derived Stromal Cells Identifies a Contractile Cell Subpopulation.

Stem Cells Int 2021 28;2021:5595172. Epub 2021 Apr 28.

Institute for Cellular and Molecular Medicine, Department of Immunology, SAMRC Extramural Unit for Stem Cell Research and Therapy, Faculty of Health Sciences, University of Pretoria, Pretoria 0001, South Africa.

The potential for human adipose-derived stromal cells (hASCs) to be used as a therapeutic product is being assessed in multiple clinical trials. However, much is still to be learned about these cells before they can be used with confidence in the clinical setting. An inherent characteristic of hASCs that is not well understood is their heterogeneity. 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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Spermidine inhibits vascular calcification in chronic kidney disease through modulation of SIRT1 signaling pathway.

Aging Cell 2021 Jun 9;20(6):e13377. Epub 2021 May 9.

Department of Cardiology, Laboratory of Heart Center, Heart Center, Zhujiang Hospital, Southern Medical University, Guangzhou, China.

Vascular calcification is a common pathologic condition in patients with chronic kidney disease (CKD) and aging individuals. It has been established that vascular calcification is a gene-regulated biological process resembling osteogenesis involving osteogenic differentiation. However, there is no efficient treatment available for vascular calcification so far. Read More

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AMPA-Type Glutamate Receptors Associated With Vascular Smooth Muscle Cell Subpopulations in Atherosclerosis and Vascular Injury.

Front Cardiovasc Med 2021 20;8:655869. Epub 2021 Apr 20.

Laboratory of Immunobiology, Center for Bioelectronic Medicine, Department of Medicine, Center for Molecular Medicine, Karolinska Institute, Stockholm, Sweden.

Vascular smooth muscle cells (VSMCs) are key constituents of both normal arteries and atherosclerotic plaques. They have an ability to adapt to changes in the local environment by undergoing phenotypic modulation. An improved understanding of the mechanisms that regulate VSMC phenotypic changes may provide insights that suggest new therapeutic targets in treatment of cardiovascular disease (CVD). Read More

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Oxidant-resistant LRRC8A/C anion channels support superoxide production by NADPH oxidase 1.

J Physiol 2021 Jun 26;599(12):3013-3036. Epub 2021 May 26.

Department of Pediatrics, Vanderbilt University Medical Center, Nashville, TN, 37232, USA.

Key Points: LRRC8A-containing anion channels associate with NADPH oxidase 1 (Nox1) and regulate superoxide production and tumour necrosis factor-α (TNFα) signalling. Here we show that LRRC8C and 8D also co-immunoprecipitate with Nox1 in vascular smooth muscle cells. LRRC8C knockdown inhibited TNFα-induced O production, receptor endocytosis, nuclear factor-κB (NF-κB) activation and proliferation while LRRC8D knockdown enhanced NF-κB activation. Read More

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Mass Spectrometry Imaging as a Tool to Investigate Region Specific Lipid Alterations in Symptomatic Human Carotid Atherosclerotic Plaques.

Metabolites 2021 Apr 18;11(4). Epub 2021 Apr 18.

Fondazione Pisana per la Scienza ONLUS, 56017 San Giuliano Terme (PI), Italy.

Atherosclerosis is characterized by fatty plaques in large and medium sized arteries. Their rupture can causes thrombi, occlusions of downstream vessels and adverse clinical events. The investigation of atherosclerotic plaques is made difficult by their highly heterogeneous nature. Read More

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LINC01278 Sponges miR-500b-5p to Regulate the Expression of ACTG2 to Control Phenotypic Switching in Human Vascular Smooth Muscle Cells During Aortic Dissection.

J Am Heart Assoc 2021 May 29;10(9):e018062. Epub 2021 Apr 29.

Department of Cardiovascular Surgery of the Second Hospital of Jilin University Changchun Jilin China.

Background Phenotypic switching in vascular smooth muscle cells (VSMCs) is involved in the pathogenesis of aortic dissection (AD). This study aims to explore the potential mechanisms of linc01278 during VSMC phenotypic switching. Methods and Results Twelve samples (6 AD and 6 control) were used for lncRNA, microRNA, and mRNA microarray analysis. Read More

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[New insights into vascular mechanobiology: roles of matrix mechanics in regulating smooth muscle cell function].

Sheng Li Xue Bao 2021 Apr;73(2):160-174

Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing 100191, China.

Vascular smooth muscle cell (vSMC) is the predominant cell type in the blood vessel wall and is constantly subjected to a complex extracellular microenvironment. Mechanical forces that are conveyed by changes in stiffness/elasticity, geometry and topology of the extracellular matrix have been indicated by experimental studies to affect the phenotype and function of vSMCs. vSMCs perceive the mechanical stimuli from matrix via specialized mechanosensors, translate these stimuli into biochemical signals controlling gene expression and activation, with the consequent modulation in controlling various aspects of SMC behaviors. Read More

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miR-145 micelles mitigate atherosclerosis by modulating vascular smooth muscle cell phenotype.

Biomaterials 2021 06 9;273:120810. Epub 2021 Apr 9.

Department of Biomedical Engineering, University of Southern California, Los Angeles, CA, 90089, United States; Division of Vascular Surgery and Endovascular Therapy, Department of Surgery, Keck School of Medicine, University of Southern California, Los Angeles, CA, 90033, United States; Mork Family Department of Chemical Engineering and Materials Science, University of Southern California, Los Angeles, CA, 90089, United States; Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research, Keck School of Medicine, University of Southern California, Los Angeles, CA, 90033, United States; Division of Nephrology and Hypertension, Department of Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA, 90033, United States; Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, 90089, United States. Electronic address:

In atherosclerosis, resident vascular smooth muscle cells (VSMCs) in the blood vessels become highly plastic and undergo phenotypic switching from the quiescent, contractile phenotype to the migratory and proliferative, synthetic phenotype. Additionally, recent VSMC lineage-tracing mouse models of atherosclerosis have found that VSMCs transdifferentiate into macrophage-like and osteochondrogenic cells and make up to 70% of cells found in atherosclerotic plaques. Given VSMC phenotypic switching is regulated by microRNA-145 (miR-145), we hypothesized that nanoparticle-mediated delivery of miR-145 to VSMCs has the potential to mitigate atherosclerosis development by inhibiting plaque-propagating cell types derived from VSMCs. Read More

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Urantide alleviates the symptoms of atherosclerotic rats in vivo and in vitro models through the JAK2/STAT3 signaling pathway.

Eur J Pharmacol 2021 Jul 20;902:174037. Epub 2021 Apr 20.

Department of Pathophysiology, Chengde Medical University, Chengde, Hebei, 067000, China. Electronic address:

Atherosclerosis is the leading cause of human death, and its occurrence and development are related to the urotensin II (UII) and UII receptor (UT) system and the biological function of vascular smooth muscle cells (VSMCs). During atherosclerosis, impaired biological function VSMCs may promote atherosclerotic plaque formation. The Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway is an important mediator of signal transduction; however, the role of this signaling pathway in atherosclerosis and VSMCs remains unknown. Read More

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MiR-506-3p Promotes the Proliferation and Migration of Vascular Smooth Muscle Cells via Targeting KLF4.

Pathobiology 2021 Apr 21:1-12. Epub 2021 Apr 21.

Department of Physiology & Pathophysiology, Xi'an Jiaotong University School of Basic Medical Sciences, Xi'an, China.

Background: The dysregulation of proliferation and migration of vascular smooth muscle cells (VSMCs) is one of the major causes of atherosclerosis (AS). Accumulating studies confirm that Kruppel-like factor 4 (KLF4) can regulate the proliferation and differentiation of VSMCs through multiple signaling pathways. However, the mechanism of KLF4 dysregulation remains unknown. Read More

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SM22 Loss Contributes to Apoptosis of Vascular Smooth Muscle Cells via Macrophage-Derived circRasGEF1B.

Oxid Med Cell Longev 2021 16;2021:5564884. Epub 2021 Mar 16.

Department of Biochemistry and Molecular Biology, College of Basic Medicine, Key Laboratory of Medical Biotechnology of Hebei Province, Hebei Medical University, Shijiazhuang, Hebei 050017, China.

Vascular smooth muscle cell (VSMC) apoptosis is a major defining feature of abdominal aortic aneurysm (AAA) and mainly caused by inflammatory cell infiltration. Smooth muscle (SM) 22 prevents AAA formation through suppressing NF-B activation. However, the role of SM22 in VSMC apoptosis is controversial. Read More

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Lysosome (Dys)function in Atherosclerosis-A Big Weight on the Shoulders of a Small Organelle.

Front Cell Dev Biol 2021 29;9:658995. Epub 2021 Mar 29.

iNOVA4Health, Chronic Diseases Research Center (CEDOC), NOVA Medical School (NMS), Universidade NOVA de Lisboa, Lisbon, Portugal.

Atherosclerosis is a progressive insidious chronic disease that underlies most of the cardiovascular pathologies, including myocardial infarction and ischemic stroke. The malfunctioning of the lysosomal compartment has a central role in the etiology and pathogenesis of atherosclerosis. Lysosomes are the degradative organelles of mammalian cells and process endogenous and exogenous substrates in a very efficient manner. Read More

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Bone marrow-derived AXL tyrosine kinase promotes mitogenic crosstalk and cardiac allograft vasculopathy.

J Heart Lung Transplant 2021 Jun 13;40(6):435-446. Epub 2021 Mar 13.

Department of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois; Department of Pediatrics, Feinberg School of Medicine, Northwestern University, Chicago, Illinois; The Heart Center, Stanley Manne Children's Research Institute, Lurie Children's Hospital, Chicago, Illinois. Electronic address:

Cardiac Allograft Vasculopathy (CAV) is a leading contributor to late transplant rejection. Although implicated, the mechanisms by which bone marrow-derived cells promote CAV remain unclear. Emerging evidence implicates the cell surface receptor tyrosine kinase AXL to be elevated in rejecting human allografts. Read More

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Circular RNA circ-ARFIP2 regulates proliferation, migration and invasion in human vascular smooth muscle cells via miR-338-3p-dependent modulation of KDR.

Metab Brain Dis 2021 Apr 10. Epub 2021 Apr 10.

Department of Neurosurgery, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, No.106 Zhongshan Second Road, Guangzhou, 510000, Guangdong, China.

Dysfunction of vascular smooth muscle cells (VSMCs) plays a critical role in the pathogenesis of intracranial aneurysm (IA). Circular RNAs (circRNAs) have been implicated in the pathogenesis of IA by reducing microRNA (miRNA) activity. In this paper, we investigated the precise roles of circRNA ADP ribosylation factor interacting protein 2 (circ-ARFIP2, circ_0021001) in VSMC dysfunction. Read More

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