LncRNA MALAT1 modulates ox-LDL induced EndMT through the Wnt/β-catenin signaling pathway

Li, Hongrong; Zhao, Qifei; Chang, Liping; Wang, Cong; Bei, Hongying; Yin, Yuehui; Chen, Meng; Wang, Hongtao; Liang, Jing; Wu, Yiling

doi:10.1186/s12944-019-1006-7

Cited by 70 publications

(51 citation statements)

References 54 publications

(65 reference statements)

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“…The SNPs in MALAT1 were associated with CVD risk in a Chinese population . MALAT1 was also found up‐regulated in patients with unstable angina and high‐fat food fed ApoE −/− mice, indicating MALAT1 participated in development of atherosclerosis . Knockdown of MALAT1 caused increased plaque size and infiltration of inflammatory CD45 + cells partly via regulation of miR‐503 .…”

Section: Malat1 and Vascular Diseasesmentioning

confidence: 94%

“…Knockdown of MALAT1 caused increased plaque size and infiltration of inflammatory CD45 + cells partly via regulation of miR‐503 . Furthermore, MALAT1 were also involved in regulation of endothelial dysfunction, lipid accumulation and chronic inflammation, which contributed to development of atherosclerosis …”

Section: Malat1 and Vascular Diseasesmentioning

confidence: 99%

“…Ox‐LDL is considered to be a key factor of initiating and accelerating atherosclerosis and induce the endothelium dysfunction . Ox‐LDL induced MALAT1 and dysfunction of HUVECs by increasing endothelial‐to‐mesenchymal transition (EndMT) via activation of Wnt/β‐catenin signaling, which is common in mouse atherosclerotic lesions and associated with plaque instability in the clinical events . Another study revealed that MALAT1 up‐regulated EndMT expression by sponging miR‐145, which was reported to inhibit SMAD3‐mediated EndMT .…”

Section: Malat1 and Vascular Diseasesmentioning

confidence: 99%

“…39 MALAT1 was also found up-regulated in patients with unstable angina and high-fat food fed ApoE −/− mice, indicating MALAT1 participated in development of atherosclerosis. 35,40 Knockdown of MALAT1 caused increased plaque size and infiltration of inflammatory CD45 + cells partly via regulation of miR-503. 41 Furthermore, MALAT1 were also involved in regulation of endothelial dysfunction, lipid accumulation and chronic inflammation, which contributed to development of atherosclerosis.…”

Section: Malat1 and Atherosclerosismentioning

confidence: 99%

“…41 Furthermore, MALAT1 were also involved in regulation of endothelial dysfunction, lipid accumulation and chronic inflammation, which contributed to development of atherosclerosis. 40,42,43…”

Section: Malat1 and Atherosclerosismentioning

confidence: 99%

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The role of lncRNA MALAT1 in cardiovascular disease

Yan

Song

et al. 2019

IUBMB Life

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Cardiovascular disease (CVD) is the first leading cause of death worldwide. Understanding the molecular mechanism of signaling pathways involved in pathology of CVD is benefit for targeted therapeutics. Recently, long non‐coding RNAs (lncRNAs) are found and involved in regulation of pathology of CVD at different levels. Among them, MALAT1 attracted more attention as it was profoundly expressed in endothelial cells or cardiomyocytes in response to the risk factors of CVD, such as hypoxia, high glucose, cytokine, and oxidative stress. In this review, we summarize recent progresses in research on the molecular mechanism of MALAT1 on regulating the pathophysiological processes of CVD as well as its potential therapeutic applications.

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Section: Malat1 and Vascular Diseasesmentioning

confidence: 94%

Section: Malat1 and Vascular Diseasesmentioning

confidence: 99%

Section: Malat1 and Vascular Diseasesmentioning

confidence: 99%

Section: Malat1 and Atherosclerosismentioning

confidence: 99%

Section: Malat1 and Atherosclerosismentioning

confidence: 99%

See 3 more Smart Citations

The role of lncRNA MALAT1 in cardiovascular disease

Yan

Song

et al. 2019

IUBMB Life

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A novel circulating biomarker lnc‐MALAT1 for acute myocardial infarction: Its relationship with disease risk, features, cytokines, and major adverse cardiovascular events

Jin

Liu

et al. 2022

Clinical Laboratory Analysis

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Objective Long noncoding RNA MALAT1 (lnc‐MALAT1) modulates atherosclerotic progression, myocardial ischemia injury, and systematic inflammation, which may be closely involved in acute myocardial infarction (AMI) pathogenesis. Thus, the current study intended to explore the relationship of lnc‐MALAT1 to disease risk, features, cytokines, and prognostication in AMI patients. Methods This multicenter study consecutively enrolled 160 newly diagnosed AMI patients and 50 controls (angina pectoris patients). Their peripheral blood mononuclear cells were obtained to measure lnc‐MALAT1 by RT–qPCR. Serum cytokines in AMI patients were detected by ELISA. In addition, AMI patients were followed up for major adverse cardiovascular event (MACE) risk evaluation. Results Lnc‐MALAT1 was higher in AMI patients than in controls (median: 2.245 vs. 0.996, p = 0.004), and it also presented a good capacity for differentiating AMI patients from controls with an area under the curve of 0.823. Lnc‐MALAT1 was positively related to C‐reactive protein (p = 0.005), low‐density lipoprotein cholesterol (p = 0.022), cardiac troponin I (p = 0.021), and infarct size (p = 0.007), but not other biochemical indexes in AMI patients. Meanwhile, lnc‐MALAT1 was positively associated with tumor necrosis factor‐alpha (p = 0.001), interleukin (IL)‐6 (p = 0.031), IL‐17A (p = 0.042), vascular cell adhesion molecule‐1 (p = 0.004), and intercellular adhesion molecule‐1 (p = 0.021) among AMI patients. Importantly, after categorization, lnc‐MALAT1 high (vs. low) was related to an elevated MACE accumulation rate (p = 0.035); furthermore, a higher lnc‐MALAT1 quartile showed a trend to be linked with an increased MACE accumulation rate (p = 0.092). Conclusion Lnc‐MALAT1 may serve as a biomarker for AMI risk, infarct size, inflammation and prognosis, but further validation by large‐scale studies is needed.

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Regulatory Non-coding RNAs in Atherosclerosis

Schober

Maleki

Nazari-Jahantigh

2020

Handbook of Experimental Pharmacology

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Regulatory RNAs like microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) control vascular and immune cells’ phenotype and thus play a crucial role in atherosclerosis. Moreover, the mutual interactions between miRNAs and lncRNAs link both types of regulatory RNAs in a functional network that affects lesion formation. In this review, we deduce novel concepts of atherosclerosis from the analysis of the current data on regulatory RNAs’ role in endothelial cells (ECs) and macrophages. In contrast to arterial ECs, which adopt a stable phenotype by adaptation to high shear stress, macrophages are highly plastic and quickly change their activation status. At predilection sites of atherosclerosis, such as arterial bifurcations, ECs are exposed to disturbed laminar flow, which generates a dysadaptive stress response mediated by miRNAs. Whereas the highly abundant miR-126-5p promotes regenerative proliferation of dysadapted ECs, miR-103-3p stimulates inflammatory activation and impairs endothelial regeneration by aberrant proliferation and micronuclei formation. In macrophages, miRNAs are essential in regulating energy and lipid metabolism, which affects inflammatory activation and foam cell formation.Moreover, lipopolysaccharide-induced miR-155 and miR-146 shape inflammatory macrophage activation through their oppositional effects on NF-kB. Most lncRNAs are not conserved between species, except a small group of very long lncRNAs, such as MALAT1, which blocks numerous miRNAs by providing non-functional binding sites. In summary, regulatory RNAs’ roles are highly context-dependent, and therapeutic approaches that target specific functional interactions of miRNAs appear promising against cardiovascular diseases.

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LncRNA MALAT1 modulates ox-LDL induced EndMT through the Wnt/β-catenin signaling pathway

Cited by 70 publications

References 54 publications

The role of lncRNA MALAT1 in cardiovascular disease

The role of lncRNA MALAT1 in cardiovascular disease

A novel circulating biomarker lnc‐MALAT1 for acute myocardial infarction: Its relationship with disease risk, features, cytokines, and major adverse cardiovascular events

Regulatory Non-coding RNAs in Atherosclerosis

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