ArticleJCI insight2020
CD47 prevents the elimination of diseased fibroblasts in scleroderma.
Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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
23 citing papers in PubMed, 37 citations in OpenAlex.
- CD47 signaling in aging and age-related diseases: mechanisms, challenges, and therapeutic opportunities.Biogerontology · 2025Review
- Elevated CD47 Expression Impairs Elimination of Photoaged Fibroblasts by Macrophages and Serves as a Potential Biomarker for Photoaging.Journal of cosmetic dermatology · 2025Article
- Article
- Beyond cancer: The potential application of CD47-based therapy in non-cancer diseases.Acta pharmaceutica Sinica. B · 2025Review
- Mutual Amplification of GLI2/Hedgehog and Transcription Factor JUN/AP-1 Signaling in Fibroblasts in Systemic Sclerosis: Potential Implications for Combined Therapies.Arthritis & rheumatology (Hoboken, N.J.) · 2025Article
- The RRP9-JUN axis promotes breast cancer progression via the AKT signalling pathway.Biology direct · 2024Article
- Cancer stem cells: advances in the glucose, lipid and amino acid metabolism.Molecular and cellular biochemistry · 2024Review
- Thrombospondin-1 promotes fibro-adipogenic stromal expansion and contractile dysfunction of the diaphragm in obesity.JCI insight · 2024Article
- The Human Neonatal Skin Fibroblast, an Available Cell Source for Tissue Production and Transplantation, Exhibits Low Risk of Immunogenicity In Vitro.International journal of molecular sciences · 2024Article
- Cell Death in Liver Disease and Liver Surgery.Biomedicines · 2024Review
- IL-6 trans-signaling in a humanized mouse model of scleroderma.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Evidence of SARS-CoV-2 infection in postmortem lung, kidney, and liver samples, revealing cellular targets involved in COVID-19 pathogenesis.Archives of virology · 2023Article
- Molecular Mechanisms Behind the Role of Plasmacytoid Dendritic Cells in Systemic Sclerosis.Biology · 2023Review
- Macrophage-evading and tumor-specific apoptosis inducing nanoparticles for targeted cancer therapy.Acta pharmaceutica Sinica. B · 2023Article
- Autoimmunity, cancer and COVID-19 abnormally activate wound healing pathways: critical role of inflammation.Histochemistry and cell biology · 2022Review
- 2021 Jeffrey M. Hoeg Award Lecture: Defining the Role of Efferocytosis in Cardiovascular Disease: A Focus on the CD47 (Cluster of Differentiation 47) Axis.Arteriosclerosis, thrombosis, and vascular biology · 2022Review
- Clonal Expansion of Stem/Progenitor Cells in Cancer, Fibrotic Diseases, and Atherosclerosis, and CD47 Protection of Pathogenic Cells.Annual review of medicine · 2022Review
- JUN promotes hypertrophic skin scarring via CD36 in preclinical in vitro and in vivo models.Science translational medicine · 2021Article
- National Institutes of Health Consensus Development Project on Criteria for Clinical Trials in Chronic Graft-versus-Host Disease: IIa. The 2020 Clinical Implementation and Early Diagnosis Working Group Report.Transplantation and cellular therapy · 2021Article
- Myofibroblast fate plasticity in tissue repair and fibrosis: Deactivation, apoptosis, senescence and reprogramming.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society · 2021Article
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Scleroderma is a devastating fibrotic autoimmune disease. Current treatments are partly effective in preventing disease progression but do not remove fibrotic tissue. Here, we evaluated whether scleroderma fibroblasts take advantage of the "don't-eat-me-signal" CD47 and whether blocking CD47 enables the body's immune system to get rid of diseased fibroblasts. To test this approach, we used a Jun-inducible scleroderma model. We first demonstrated in patient samples that scleroderma upregulated transcription factor JUN and increased promoter accessibilities of both JUN and CD47. Next, we established our scleroderma model, demonstrating that Jun mediated skin fibrosis through the hedgehog-dependent expansion of CD26+Sca1- fibroblasts in mice. In a niche-independent adaptive transfer model, JUN steered graft survival and conferred increased self-renewal to fibroblasts. In vivo, JUN enhanced the expression of CD47, and inhibiting CD47 eliminated an ectopic fibroblast graft and increased in vitro phagocytosis. In the syngeneic mouse, depleting macrophages ameliorated skin fibrosis. Therapeutically, combined CD47 and IL-6 blockade reversed skin fibrosis in mice and led to the rapid elimination of ectopically transplanted scleroderma cells. Altogether, our study demonstrates the efficiency of combining different immunotherapies in treating scleroderma and provides a rationale for combining CD47 and IL-6 inhibition in clinical trials.
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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.