ArticleJCI insight2019
Long noncoding RNA Malat1 regulates differential activation of macrophages and response to lung injury.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
84 citing papers in PubMed, 136 citations in OpenAlex.
- The Relationship Between Differential Expression of Non-coding RNAs (TP53TG1, LINC00342, MALAT1, DNM3OS, miR-126-3p, miR-200a-3p, miR-18a-5p) and Protein-Coding Genes (PTEN, FOXO3) and Risk of Idiopathic Pulmonary Fibrosis.Biochemical genetics · 2026Article
- Macrophage Phenotypic Plasticity and Inflammatory Mechanisms in Hyperoxia-Induced Lung Injury.Journal of inflammation research · 2026Review
- Human lncRNA, hLinfRNA7 (IDO1-AS) Regulates Cytokine Expression, Tryptophan Catabolism, and Inflammatory Response in Macrophage.Molecular and cellular biology · 2026Article
- Modulation of NEAT1 and MALAT1 expression in WJ-MSCs by Covid-19 serum: a foundation for EVs-mediated therapy.Respiratory research · 2025Article
- Targeting long non-coding RNAMolecular therapy. Nucleic acids · 2025Article
- Long non-coding RNAMolecular therapy. Nucleic acids · 2025Review
- Emodin Alleviates Acute Pancreatitis-Associated Acute Lung Injury by Inhibiting Serum Exosomal miRNA-21-3p-Induced M1 Alveolar Macrophage Polarisation.Journal of cellular and molecular medicine · 2025Article
- Innate immune memory in macrophage differentiation and cardiovascular diseases.Inflammation and regeneration · 2025Review
- Review
- scRNA-seq uncovers the transcriptional dynamics of Encephalitozoon intestinalis parasites in human macrophages.Nature communications · 2025Article
- ANKRD22 participates in the proinflammatory activities of macrophages in the colon cancer tumor microenvironment.Cancer immunology, immunotherapy : CII · 2025Article
- Biological functions and affected signaling pathways by Long Non-Coding RNAs in the immune system.Non-coding RNA research · 2025Review
- Multi-omics identification and validation of oxidative phosphorylation-related hub genes in schizophrenia.Frontiers in genetics · 2025Article
- Progress of alveolar macrophages in biological function and acute lung injury/acute respiratory distress syndrome.Frontiers in immunology · 2025Review
- MALAT1 and HIST1H2BC as connecting diagnostic biomarkers in Ebola and its overlapping disease: An integrative approach.Bioinformation · 2025Article
- Immune mechanisms and novel therapies for idiopathic pulmonary fibrosis.Pharmaceutical science advances · 2024Review
- Suppression of the JAK/STAT pathway inhibits neuroinflammation in the line 61-PFF mouse model of Parkinson's disease.Journal of neuroinflammation · 2024Article
- Suppression of the JAK/STAT Pathway Inhibits Neuroinflammation in the Line 61-PFF Mouse Model of Parkinson's Disease.Research square · 2024Article
- Non-coding RNAs in disease: from mechanisms to therapeutics.Nature reviews. Genetics · 2024Review
- Roles of lncRNAs in NF-κB-Mediated Macrophage Inflammation and Their Implications in the Pathogenesis of Human Diseases.International journal of molecular sciences · 2024Review
24 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
Abstract
Macrophage activation, i.e., classical M1 and the alternative M2, plays a critical role in many pathophysiological processes, such as inflammation and tissue injury and repair. Although the regulation of macrophage activation has been under extensive investigation, there is little knowledge about the role of long noncoding RNAs (lncRNAs) in this event. In this study, we found that lncRNA Malat1 expression is distinctly regulated in differentially activated macrophages in that it is upregulated in LPS-treated and downregulated in IL-4-treated cells. Malat1 knockdown attenuates LPS-induced M1 macrophage activation. In contrast, Malat1 knockdown enhanced IL-4-activated M2 differentiation as well as a macrophage profibrotic phenotype. Mechanistically, Malat1 knockdown led to decreased expression of Clec16a, silencing of which phenocopied the regulatory effect of Malat1 on M1 activation. Interestingly, Malat1 knockdown promoted IL-4 induction of mitochondrial pyruvate carriers (MPCs) and their mediation of glucose-derived oxidative phosphorylation (OxPhos), which was crucial to the Malat1 regulation of M2 differentiation and profibrotic phenotype. Furthermore, mice with either global or conditional myeloid knockout of Malat1 demonstrated diminished LPS-induced systemic and pulmonary inflammation and injury. In contrast, these mice developed more severe bleomycin-induced lung fibrosis, accompanied by alveolar macrophages displaying augmented M2 and profibrotic phenotypes. In summary, we have identified what we believe is a previously unrecognized role of Malat1 in the regulation of macrophage polarization. Our data demonstrate that Malat1 is involved in pulmonary pathogeneses in association with aberrant macrophage activation.
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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.