6,779 results match your criteria 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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Dexamethasone reduces the formation of thoracic aortic aneurysm and dissection in a murine model.

Exp Cell Res 2021 Jun 10:112703. Epub 2021 Jun 10.

Department of Vascular Surgery, Peking University People's Hospital, Beijing, People's Republic of China. Electronic address:

Thoracic aortic aneurysm and dissection (TAAD) is a life-threatening vascular disease with no effective pharmaceutical therapies currently available. Inflammation plays a key role in the progression of aneurysms. Dexamethasone (DEX), a synthetic glucocorticoid, has showed alleviating effects on cells in vitro from TAAD patients. 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

LncRNA SAMMSON Overexpression Suppresses Vascular Smooth Muscle Cell Proliferation via Inhibiting miR-130a Maturation to Participate in Intracranial Aneurysm.

Neuropsychiatr Dis Treat 2021 4;17:1793-1799. Epub 2021 Jun 4.

Department of Neurosurgery West China Hospital, Sichuan University, Chengdu Province, 610041, People's Republic of China.

Background: MiR-130a is a recently identified critical player in vascular smooth muscle cell (VSMC) proliferation, which participates in intracranial aneurysm (IA). However, the involvement of miR-130a in IA and its upstream regulator are unknown. Our preliminary sequencing analysis revealed a close correlation between miR-130a and lncRNA SAMMSON across IA samples. Read More

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CD38 deficiency alleviates Ang II-induced vascular remodeling by inhibiting small extracellular vesicle-mediated vascular smooth muscle cell senescence in mice.

Signal Transduct Target Ther 2021 Jun 11;6(1):223. Epub 2021 Jun 11.

The National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Nanchang University, Nanchang, People's Republic of China.

CD38 is the main enzyme for nicotinamide adenine dinucleotide (NAD) degradation in mammalian cells. Decreased NAD levels are closely related to metabolic syndromes and aging-related diseases. Our study showed that CD38 deficiency significantly alleviated angiotensin II (Ang II)-induced vascular remodeling in mice, as shown by decreased blood pressures; reduced vascular media thickness, media-to-lumen ratio, and collagen deposition; and restored elastin expression. 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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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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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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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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Anti-Atherosclerotic Effect of Afrocyclamin A against Vascular Smooth Muscle Cells Is Mediated via p38 MAPK Signaling Pathway.

Cell J 2021 Jul 26;23(2):191-198. Epub 2021 May 26.

Department of General Surgery, Shanghai Fourth People's Hospital Affiliated to Tongji University School of Medicine, Shanghai, China.

Objective: Research suggests that fine particulate matter (PM2.5) contributes to the expansion and development of atherosclerosis. Infiltration and proliferation of vascular smooth muscle cells (VSMCs) from the blood vessel media into the intima, is an important step in the atherosclerosis pathophysiology. 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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Sterol-resistant SCAP Overexpression in Vascular Smooth Muscle Cells Accelerates Atherosclerosis by Increasing Local Vascular Inflammation through Activation of the NLRP3 Inflammasome in Mice.

Aging Dis 2021 Jun 1;12(3):747-763. Epub 2021 Jun 1.

1Centre for Lipid Research & Key Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, the Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.

Atherosclerosis is a serious age-related pathology, and one of its hallmarks is the presence of chronic inflammation. Sterol regulatory element-binding protein (SREBP) cleavage-activating protein (SCAP) is a cholesterol sensor that plays an essential role in regulating intracellular cholesterol homeostasis. Accordingly, dysregulation of the SCAP-SREBP pathway has been reported to be closely associated with an increased risk of obesity, hypercholesterolemia, and cardiovascular disease. 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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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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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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The ameliorative effect of terpinen-4-ol on ER stress-induced vascular calcification depends on SIRT1-mediated regulation of PERK acetylation.

Pharmacol Res 2021 Jun 3;170:105629. Epub 2021 Jun 3.

The State Key Laboratory of Functions and Applications of Medicinal Plants, Guizhou Medical University, University Town, Guian New District, Guizhou, China; Department of Pharmacology of Materia Medica (The High Educational Key Laboratory of Guizhou Province for Natural Medicinal Pharmacology and Druggability, The High Efficacy Application of Natural Medicinal Resources Engineering Center of Guizhou Province), Guizhou Medical University, University Town, Guian New District, Guizhou, China; The Key Laboratory of Optimal Utilization of Natural Medicine Resources, School of Pharmaceutical Sciences, Guizhou Medical University, University Town, Guian New District, Guizhou, China. Electronic address:

Endoplasmic reticulum (ER) stress-mediated phenotypic switching of vascular smooth muscle cells (VSMCs) is key to vascular calcification (VC) in patients with chronic kidney disease (CKD). Studies have shown that activation/upregulation of SIRT1 has a protective effect on CKD-VC. Meanwhile, although terpinen-4-ol has been shown to exert a protective effect against cardiovascular disease, its role and underlying mechanism in VC remain unclear. 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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Nano-Sized Hydroxyapatite Induces Apoptosis and Osteogenic Differentiation of Vascular Smooth Muscle Cells via JNK/c-JUN Pathway.

Int J Nanomedicine 2021 27;16:3633-3648. Epub 2021 May 27.

Department of Cardiology, Cardiovascular Key Laboratory of Zhejiang Province, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang Province, 310009, People's Republic of China.

Purpose: The deposition of hydroxyapatite (HAp) crystals plays an important role in the development of vascular calcification (VC). This study aimed to demonstrate the effects of nanosized HAp (nHAp) on vascular smooth muscle cells (VSMCs) and VC progression.

Methods: Transmission electron microscopy (TEM) was used to examine cellular uptake of nHAp. Read More

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Abnormal Pressure Stress Reduces Interleukin-1β-Induced Cyclooxygenase-2 Expression in Cultured Rat Vascular Smooth Muscle Cells.

Biol Pharm Bull 2021 ;44(6):853-860

Department of Pharmacological Sciences, School of Pharmaceutical Sciences, Health Sciences University of Hokkaido.

Elevated mechanical stress on blood vessels associated with hypertension has a direct effect on the function of vascular endothelial cells and vascular smooth muscle cells (VSMCs). In the present study, we have identified the effect of pulsatile pressure stress on cyclooxygenase-2 (COX-2) expression induced by interleukin (IL)-1β in cultured rat VSMCs. VSMCs were isolated from aortic media of Wistar rats and cultured. Read More

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January 2021

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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