ArticleJCI insight2022
KLF4 is a therapeutically tractable brake on fibroblast activation that promotes resolution of pulmonary fibrosis.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
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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.
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Who cites it
25 citing papers in PubMed, 33 citations in OpenAlex.
- Decoding fibroblast activation: Transcriptional networks in hepatic stellate cells and across fibrotic organs (Review).International journal of molecular medicine · 2026Review
- MRC2-mediated collagen internalization is reduced in fibrotic lung fibroblasts and increased upon phenotypic dedifferentiation.JCI insight · 2026Article
- Conserved Transcriptional Circuits Regulate Cardiac Fibroblast-Mediated Fibrosis.Circulation research · 2026Article
- Article
- Key role of transcription factors network in proliferative vitreoretinal diseases development.Cell & bioscience · 2026Review
- Clec3b⁺ fibroblasts are the primary effectors of portal fibrosis following activation via a KLF4/periostin axis.Nature communications · 2026Article
- Longitudinal Single-Cell RNA-seq Profiling of Lung Cell Phenotypes, Signaling, and Cross-talk During Fibrosis Resolution.bioRxiv : the preprint server for biology · 2026Article
- Osteoprotegerin-Enabled Immune Evasion of Pathological Adipose Stromal Cells Drives Metabolic Dysfunction in Obesity.bioRxiv : the preprint server for biology · 2026Article
- Zinc-Induced PKCδ-dependent Phosphorylation of MTF-1 Promotes Pulmonary Vascular Remodeling in Hypoxic Pulmonary Hypertension.International journal of biological sciences · 2026Article
- Innate Immune-Cloaked Microgel-Coated Mesenchymal Stromal Cells Reverse Persistent Pulmonary Fibrosis via Reparative Macrophages.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- Mechanistic basis for the antifibrotic actions of cAMP-based therapies.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Comprehensive transcription factor perturbations recapitulate fibroblast transcriptional states.Nature genetics · 2025Article
- Reimagining Fibrosis Research, Outcomes, and Therapeutics Through the Lens of Resolution.Seminars in respiratory and critical care medicine · 2025Review
- Distinct cAMP Regulation in Scleroderma Lung and Skin Myofibroblasts Governs Their Dedifferentiation via p38α Inhibition.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Telomeres, telomerase, and cancer: mechanisms, biomarkers, and therapeutics.Experimental hematology & oncology · 2025Review
- Recent progress in exosomal non-coding RNAs research related to idiopathic pulmonary fibrosis.Frontiers in genetics · 2025Review
- MBNL2 promotes aging-related cardiac fibrosis via inhibited SUMOylation of Krüppel-like factor4.iScience · 2024Article
- MAPK phosphatase 1 inhibition of p38α within lung myofibroblasts is essential for spontaneous fibrosis resolution.The Journal of clinical investigation · 2024Article
- The Effect ofJournal of experimental pharmacology · 2024Article
- Development of a long term, ex vivo, patient-derived explant model of endometrial cancer.PloS one · 2024Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
There is a paucity of information about potential molecular brakes on the activation of fibroblasts that drive tissue fibrosis. The transcription factor Krüppel-like factor 4 (KLF4) is best known as a determinant of cell stemness and a tumor suppressor. We found that its expression was diminished in fibroblasts from fibrotic lung. Gain- and loss-of-function studies showed that KLF4 inhibited fibroblast proliferation, collagen synthesis, and differentiation to myofibroblasts, while restoring their sensitivity to apoptosis. Conditional deletion of KLF4 from fibroblasts potentiated the peak degree of pulmonary fibrosis and abrogated the subsequent spontaneous resolution in a model of transient fibrosis. A small molecule inducer of KLF4 was able to restore its expression in fibrotic fibroblasts and elicit resolution in an experimental model characterized by more clinically relevant persistent pulmonary fibrosis. These data identify KLF4 as a pivotal brake on fibroblast activation whose induction represents a therapeutic approach in fibrosis of the lung and perhaps other organs.
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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.