ArticleProceedings of the National Academy of Sciences of the United States of America2025
Setdb1 ablation in macrophages attenuates fibrosis in heart allografts.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. 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 5 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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Who cites it
5 citing papers in PubMed.
- Platelet-derived serotonin epigenetically programs macrophage alternative activation to orchestrate type 2 airway inflammation.Cellular & molecular immunology · 2026Article
- The role of histone methylation in fibrosis and its therapeutic potential.Journal of translational medicine · 2026Review
- Macrophage metabolic reprogramming in organ transplantation: mechanisms, transplant outcomes, and therapeutic implications.Frontiers in cellular and infection microbiology · 2026Review
- The gene regulatory networks shaping macrophage plasticity and altered function in fibrosis.Frontiers in immunology · 2026Review
- Multi-omics and machine learning identify FN1 and ALDH2 as diagnostic biomarkers and therapeutic targets in early and late diabetic kidney disease.Renal failure · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
14 authors.
Funding
Abstract
Tissue fibrosis is commonly associated with organ malfunction and is strongly associated with the development of chronic rejection, cardiovascular diseases, and other chronic diseases. Fibrosis also contributes to immune exclusion in tumor tissues. Targeting fibrosis might be a strategy for prolonging allograft survival while suppressing cancer development. Here, single-cell transcriptomes of human and mouse heart allografts showed that macrophages accumulated in grafts with fibrosis were reprogrammed via histone methylation regulated by Setdb1, an H3K9 methyltransferase. Myeloid-specific deletion of Setdb1 prolonged heart allograft survival but reversed immune exclusion in tumor tissues. Interestingly, myeloid-specific Setdb1-knockout led to lower fibrosis in heart allografts and tumor tissues in mice. Our single-cell sequencing data showed that Setdb1 ablation impaired Fn1
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