ArticleNature communications2024
ALKBH5-mediated m6A modification of IL-11 drives macrophage-to-myofibroblast transition and pathological cardiac fibrosis in mice.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 80 papers, 1 of them a synthesis that pooled it.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
80 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.
- Bibliometric analysis of RNA-binding proteins in osteosarcoma: unraveling research trends and hotspots.Frontiers in immunology · 2025Pooled it
- Single-cell landscape of piglet lung response withVirulence · 2026Article
- ALKBH5 activates creatine-driven thermogenesis by stabilizing CKB mRNA in response to cold.Nature metabolism · 2026Article
- ALKBH5 Positively Regulates BMP2 to Influence Endometrial Decidualization in Recurrent Spontaneous Abortion.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Spatial multi omic profiling maps hypoxia-driven pro-fibrotic SPP1Experimental hematology & oncology · 2026Article
- Beyond EMT: Mesenchymal drift as an emerging driver of stromal-immune reprogramming in prostate cancer.iScience · 2026Review
- Macrophage-to-Myofibroblast Transdifferentiation Contributes to Pulmonary Fibrosis via the MERTK-SPP1-SRC-TKS5 Signaling Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Functional Role of ALKBH5 in Kidney Injury: Insights Into Mechanisms and Therapeutic Potential.Journal of cellular biochemistry · 2026Review
- PYRIN mActa pharmacologica Sinica · 2026Article
- MFAP4 Promotes Scar Formation by Regulating Macrophage-Myofibroblast Transformation Through Activation of the TGF-β/Smad3 Signalling Pathway.Experimental dermatology · 2026Article
- ALKBH5 aggravates scarring after glaucoma surgery via mCell death and differentiation · 2026Article
- Intestinal epithelial PIEZO1 regulates macrophage-to-myofibroblast transition via epithelial-derived TGF-α signaling in Crohn's disease.Cell communication and signaling : CCS · 2026Article
- ALKBH5-mediated m6A demethylation of PRMT6 inhibits neuronal apoptosis and ferroptosis in Alzheimer's disease via reducing transcription of ACSL4.Cell biology and toxicology · 2026Article
- mCellular & molecular biology letters · 2026Article
- Current trends, applications, and challenges in three-dimensional bioprinting for cardiovascular disease models and therapies.iScience · 2026Review
- Maternal obesity induces macrophage to myofibroblast transition in kidneys of male offspring through a pathway driven by 20-hydroxyeicosatetraenoic acid.Nature communications · 2026Article
- The impact of inflammation, neuromodulation, and gut microbiota on developing cardiac fibrosis and hypertension.Cardiovascular research · 2026Review
- Nicotine promotes cardiac fibrosis by regulating miR-125b-5p maturation via HNRNPA2B1-mediated METTL14-dependent m⁶A methylation: therapeutic reversal by cinacalcet HCl.Journal of translational medicine · 2026Article
- m6A-Mediated epitranscriptional reprogramming drives cardiac fibrosis by suppressing PGC-1α and boosting mitochondrial fission.Journal of translational medicine · 2026Article
- M6A demethylase ALKBH5 mediated Igfbp4 mRNA m6A modification drives fibroblast activation and pathological upper airway fibrosis.Clinical and translational medicine · 2026Article
20 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
18 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac macrophage contributes to the development of cardiac fibrosis, but factors that regulate cardiac macrophages transition and activation during this process remains elusive. Here we show, by single-cell transcriptomics, lineage tracing and parabiosis, that cardiac macrophages from circulating monocytes preferentially commit to macrophage-to-myofibroblast transition (MMT) under angiotensin II (Ang II)-induced hypertension, with accompanying increased expression of the RNA N6-methyladenosine demethylases, ALKBH5. Meanwhile, macrophage-specific knockout of ALKBH5 inhibits Ang II-induced MMT, and subsequently ameliorates cardiac fibrosis and dysfunction. Mechanistically, RNA immunoprecipitation sequencing identifies interlukin-11 (IL-11) mRNA as a target for ALKBH5-mediated m6A demethylation, leading to increased IL-11 mRNA stability and protein levels. By contrast, overexpression of IL11 in circulating macrophages reverses the phenotype in ALKBH5-deficient mice and macrophage. Lastly, targeted delivery of ALKBH5 or IL-11 receptor α (IL11RA1) siRNA to monocytes/macrophages attenuates MMT and cardiac fibrosis under hypertensive stress. Our results thus suggest that the ALKBH5/IL-11/IL11RA1/MMT axis alters cardiac macrophage and contributes to hypertensive cardiac fibrosis and dysfunction in mice, and thereby identify potential targets for cardiac fibrosis therapy in patients.
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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 Socratic graph.