ArticleOncotarget2018
LncRNA MALAT1 regulates smooth muscle cell phenotype switch via activation of autophagy.
Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 52 citations in OpenAlex.
- Silencing MALAT1 represses pathological progression, inflammation, and vascular smooth muscle cell phenotype switching by regulating the SEMA3C-mediated Smad pathway in intracranial aneurysms.Frontiers in cellular neuroscience · 2026Article
- Review
- Long Non-Coding RNA Function in Smooth Muscle Cell Plasticity and Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2025Review
- Targeting PDGF/PDGFR Signaling Pathway by microRNA, lncRNA, and circRNA for Therapy of Vascular Diseases: A Narrow Review.Biomolecules · 2024Review
- Role of long noncoding RNAs in diabetes-associated peripheral arterial disease.Cardiovascular diabetology · 2024Review
- LncRNA MYLK antisense RNA 1 activates cell division cycle 42/Neutal Wiskott-Aldrich syndrome protein pathway via microRNA-101-5p to accelerate epithelial-to-mesenchymal transition of colon cancer cells.The Kaohsiung journal of medical sciences · 2024Article
- LncRNAs in oncogenic microenvironment: from threat to therapy.Frontiers in cell and developmental biology · 2024Review
- Fate mapping RNA-sequencing reveal Malat1 regulates Sca1Cellular and molecular life sciences : CMLS · 2023Article
- The mechanism and therapy of aortic aneurysms.Signal transduction and targeted therapy · 2023Review
- Hibiscus attenuates renovascular hypertension-induced aortic remodeling dose dependently: the oxidative stress role and Ang II/cyclophilin A/ERK1/2 signaling.Frontiers in physiology · 2023Article
- Noncoding RNAs in Vascular Cell Biology and Restenosis.Biology · 2022Review
- Functions of the bone morphogenetic protein signaling pathway through non-coding RNAs.Non-coding RNA research · 2022Review
- Decoding microRNA drivers in atherosclerosis.Bioscience reports · 2022Review
- Exploring the role of non-coding RNAs in autophagy.Autophagy · 2022Review
- MiR-34a-3p suppresses pulmonary vascular proliferation in acute pulmonary embolism rat by targeting DUSP1.Bioscience reports · 2022Article
- Global research trends in atherosclerosis: A bibliometric and visualized study.Frontiers in cardiovascular medicine · 2022Article
- Insights Into the Role of Platelet-Derived Growth Factors: Implications for Parkinson's Disease Pathogenesis and Treatment.Frontiers in aging neuroscience · 2022Review
- Global trends and Frontier topics about vascular smooth muscle cells phenotype switch: A bibliometric analysis from 1999 to 2021.Frontiers in pharmacology · 2022Article
- Effect of Extracellular Vesicles From Multiple Cells on Vascular Smooth Muscle Cells in Atherosclerosis.Frontiers in pharmacology · 2022Review
- Vascular smooth muscle cells in atherosclerosis: time for a re-assessment.Cardiovascular research · 2021Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular smooth muscle cells (VSMCs), switching from a differentiated to a proliferative phenotype, contribute to various vascular diseases. However, the role of long noncoding RNA metastasis-associated lung adenocarcinoma transcript 1 MALAT1 in the phenotype switching of VSMCs remains unclear. Here, we report that the knockdown of MALAT1 promotes the transformation of smooth muscle cells from a proliferative phenotype to a differentiated phenotype. MALAT1 knockdown inhibited cellular proliferation and migration, leading to significant cell cycle arrest in the G2 phase. MALAT1 was downregulated in bone morphogenetic protein-7 (BMP-7)-induced cellular differentiation, while MALAT1 was upregulated in platelet-derived growth factor-BB (PDGF-BB)-induced cellular proliferation. PDGF induced the transformation of smooth muscle cells into a proliferative phenotype accompanied by an increase in autophagy. The downregulation of MALAT1 attenuated PDGF-BB-induced proliferation and migration by inhibiting autophagy. MALAT1 could act as a competing endogenous RNA (ceRNA) to regulate autophagy-related 7 (ATG7) gene expression by sponging miR142-3p. The present study reveals a novel mechanism by which MALAT1 promotes the transformation of smooth muscle cells from contraction to synthetic phenotypes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.