Role of Lipid Accumulation and Inflammation in Atherosclerosis: Focus on Molecular and Cellular Mechanisms

Frontiers in Cardiovascular Medicine, Journal Year: 2021, Volume and Issue: 8

Published: Sept. 6, 2021

Atherosclerosis is a chronic lipid-driven and maladaptive inflammatory disease of arterial intima. It characterized by the dysfunction lipid homeostasis signaling pathways that control inflammation. This article reviews role inflammation accumulation, especially low-density lipoprotein (LDL), in pathogenesis atherosclerosis, with more emphasis on cellular mechanisms. Furthermore, this review will briefly highlight medicinal plants, long non-coding RNA (lncRNA), microRNAs pathophysiology, treatment, prevention atherosclerosis. Lipid at various levels, including receptor-mediated uptake, synthesis, storage, metabolism, efflux, its impairments are important for development The major source cholesterol accumulation wall proatherogenic modified (mLDL). Modified lipoproteins, such as oxidized (ox-LDL) LDL binding proteoglycans extracellular matrix intima blood vessels, cause aggregation particles, endothelial damage, leukocyte recruitment, foam cell formation, Inflammation key contributor to atherosclerosis participates all phases Also, several studies have shown lncRNAs appeared regulators physiological pathophysiological processes regulation HDL biogenesis, regulating smooth muscle proliferation, controlling Thus, both immune response closely linked, their molecular interact each other.

Language: Английский

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New developments in the biology of fibroblast growth factors

WIREs Mechanisms of Disease, Journal Year: 2022, Volume and Issue: 14(4)

Published: Feb. 9, 2022

Abstract The fibroblast growth factor (FGF) family is composed of 18 secreted signaling proteins consisting canonical FGFs and endocrine that activate four receptor tyrosine kinases (FGFRs 1–4) intracellular (intracellular or iFGFs) primarily function to regulate the activity voltage‐gated sodium channels other molecules. FGFs, iFGFs have been reviewed extensively by us others. In this review, we briefly summarize past reviews then focus on new developments in FGF field since our last review 2015. Some highlights 6 years include use optogenetic tools, viral vectors, inducible transgenes experimentally modulate signaling, clinical small molecule FGFR inhibitors, an expanded understanding functions for stem cell pluripotency differentiation, roles tissue homeostasis regeneration, a continuing elaboration mechanisms development, expanding appreciation neuropsychiatric diseases. This article categorized under: Cardiovascular Diseases > Molecular Cellular Physiology Neurological Congenital Stem Cells Development Cancer

Language: Английский

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Targeting epigenetics and non-coding RNAs in atherosclerosis: from mechanisms to therapeutics

Pharmacology & Therapeutics, Journal Year: 2018, Volume and Issue: 196, P. 15 - 43

Published: Nov. 13, 2018

Language: Английский

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Long Noncoding RNAs in Pathological Cardiac Remodeling: A Review of the Update Literature

BioMed Research International, Journal Year: 2019, Volume and Issue: 2019, P. 1 - 11

Published: July 1, 2019

Cardiac remodeling is a self-regulatory response of the myocardium and vasculature under stressful condition. Cardiomyocytes (CMs), vascular smooth muscle cells (VSMCs), endothelial (ECs), cardiac fibroblasts (CFs) are all involved in this process, characterized by change morphological structures mechanical/chemical activities as well metabolic patterns. Despite current development consciousness, control remains unsatisfactory, to further explore underlying mechanism seek optimal therapeutic targets still urgent need clinical practice. It now emerging that long noncoding RNAs (lncRNAs) play key regulatory roles these adverse responses: lncRNA TUG1, AK098656, TRPV1, GAS5, Giver, Lnc-Ang362 have been indicated hypertension-related remodeling, H19, UCA1, MEG3, APPAT, lincRNA-p21 atherosclerosis (AS), HIF1A-AS1 Lnc-HLTF-5 aortic aneurysm (AA). In addition, Neat1, AK139328, APF, CAIF, AK088388, CARL, MALAT1, HOTAIR, XIST, NRF postischemia myocardial while Mhrt, Chast, CHRF, ROR, Plscr4, MIAT hypertrophy, wisper, H19 extracellular matrix (ECM) reconstitution. Signaling specific miRNAs acting endogenous sponge (ceRNA) was main form regulates target gene expression during remodeling. This review will underline updates lncRNAs lncRNA-miRNA interactions maladaptive also cast light on their potential targets, hoping provide supportive background for following research.

Language: Английский

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LncRNA TUG1 regulates proliferation and apoptosis by regulating miR-148b/IGF2 axis in ox-LDL-stimulated VSMC and HUVEC

Life Sciences, Journal Year: 2020, Volume and Issue: 243, P. 117287 - 117287

Published: Jan. 8, 2020

Language: Английский

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The lncRNA TUG1/miR-145-5p/FGF10 regulates proliferation and migration in VSMCs of hypertension

Biochemical and Biophysical Research Communications, Journal Year: 2018, Volume and Issue: 501(3), P. 688 - 695

Published: May 24, 2018

Language: Английский

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Probing the links: Long non-coding RNAs and NF-κB signalling in atherosclerosis

Pathology - Research and Practice, Journal Year: 2023, Volume and Issue: 249, P. 154773 - 154773

Published: Aug. 18, 2023

Language: Английский

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Pathophysiological Functions of the lncRNA TUG1

Current Pharmaceutical Design, Journal Year: 2019, Volume and Issue: 26(6), P. 688 - 700

Published: Dec. 27, 2019

Background: Long non-coding RNAs (lncRNAs) with little or no coding capacity are associated a plethora of cellular functions, participating in various biological processes. Cumulative study lncRNA provides explanations to the physiological and pathological processes new perspectives diagnosis, prevention, treatment some clinical diseases. RNA taurine-upregulated gene 1(TUG1) is one first identified lncRNAs human disease, which actively involved processes, including regulating genes at epigenetics, transcription, post-transcription, translation, posttranslation. The aim this review was explore molecular mechanism TUG1 types Methods: In review, we summarized analyzed latest findings related physiologic pathophysiological studies were retrieved selected last six years research articles PubMed as keywords. Results: valuable that its dysregulated expression found variety exhibit aberrant malignancies. Dysregulation has been shown contribute proliferation, migration, cell cycle changes, inhibited apoptosis, drug resistance cancer cells, revealed an oncogenic role for lncRNA, but reports have downregulation lung samples compared noncancerous samples. addition, functions physiology disease (relevant endocrinology, metabolism, immunology, neurobiology) also highlighted. Finally, discuss limitations tremendous diagnostic/therapeutic potential other Conclusion: RNA-TUG1 likely served useful biomarkers therapy targets effectively applied different kinds diseases, such cardiovascular

Language: Английский

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LncRNA H19 promotes the committed differentiation of stem cells from apical papilla via miR-141/SPAG9 pathway

Cell Death and Disease, Journal Year: 2019, Volume and Issue: 10(2)

Published: Feb. 12, 2019

Abstract Long noncoding RNAs (lncRNAs) exert significant roles at transcriptional and post-transcriptional levels. Stem cells from apical papilla (SCAPs) differentiate into dentin/bone-like tissues under certain conditions. So far, whether lncRNA-H19 can affect the proliferative behaviors osteo/odontogenesis of SCAPs, as well its specific mechanism remain to be elucidated. Here, SCAPs were isolated transfected with lentiviruses or packaging vectors. Our results showed that had no effect on presented by CCK-8 assay, EdU assay flow cytometry (FCM). Furthermore, alkaline phosphatase (ALP) activity, alizarin red staining, Western blot (WB), quantitative real-time polymerase chain reaction (qRT-PCR) in vivo bone formation conducted verify biological influences H19 SCAPs. Overexpression led enhanced whereas knockdown inhibited these effects. Mechanistically, competitively bound miR-141 prevented SPAG9 miRNA-mediated degradation, thus significantly elevating phosphorylated levels p38 JNK facilitating committed differentiation Taken together, was upregulated overexpression via miR-141/SPAG9 pathway.

Language: Английский

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Silence of long intergenic noncoding RNA HOTAIR ameliorates oxidative stress and inflammation response in ox‐LDL‐treated human macrophages by upregulating miR‐330‐5p

Journal of Cellular Physiology, Journal Year: 2018, Volume and Issue: 234(4), P. 5134 - 5142

Published: Sept. 6, 2018

Evidence of the involvement long noncoding RNAs (lncRNAs) in atherosclerosis is growing but still not well characterized. Here, we concentrated on biological roles lncRNA HOX transcription antisense RNA (HOTAIR) atherosclerosis. In our study, found that oxidized low-density lipoprotein (ox-LDL) induced human macrophages THP-1 cells apoptosis dose dependently and time dependently. Meanwhile, HOTAIR was significantly increased treated with ox-LDL. Then, modulated by infection LV-short hairpin (shRNA) LV-HOTAIR into cells. As displayed, CD36, Oil Red O staining levels, total cholesterol, triglyceride levels dil-ox-LDL uptake rate were greatly repressed silence while triggered overexpression HOTAIR. Moreover, knockdown suppressed reactive oxygen species, malondialdehyde superoxide dismutase activity cell also restrained. Reversely, exhibited an opposite phenomenon. addition, interleukin 6 (IL-6), IL-1β, cyclo-oxygenase 2, tumor necrosis factor α protein depressed LV-shRNA) upregulation By carrying out bioinformatics analysis, miR-330-5p predicted as a target correlation between them validated current study. MiR-330-5p decreased incubated ox-LDL able to inhibit oxidative stress inflammation process. Taken together, it implied contributed development downregulating macrophages.

Language: Английский

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