ArticleNature cardiovascular research2025
Dynamic molecular atlas of cardiac fibrosis at single-cell resolution shows CD248 in cardiac fibroblasts orchestrates interactions with immune cells.
Article in Nature cardiovascular research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- CD248 expression in human adipose tissue is upregulated in obesity and following glucocorticoid exposure: a mediator of insulin resistance and adipose dysfunction?Molecular medicine (Cambridge, Mass.) · 2026Article
- Cardiac immunity and heart repair: Mechanism, challenge, and future direction.Chinese medical journal · 2026Review
- Review
- Shared mechanisms of organ fibrosis.JCI insight · 2026Review
- Article
- Mechanisms, precision therapies, and technological frontiers in coronary atherosclerosis: a comprehensive review.Acta pharmacologica Sinica · 2026Review
- mRNA medicine for cardiovascular disease.Nature cardiovascular research · 2026Review
- Decoding organ fibrosis: mechanistic insights and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Deletion of Cd248 inJournal of molecular and cellular cardiology plus · 2026Article
- Interconnected Pathways and Therapeutic Implications for Cardiovascular Aging and Diseases.JACC. Asia · 2026Review
- Engineered T cell therapy for the treatment of cardiac fibrosis during chronic phase of myocarditis.Theranostics · 2026Article
- Cardiac fibroblast heterogeneity in cardiac fibrosis implication for cell-type-specific treatment.Frontiers in physiology · 2026Review
- Cardiovascular toxicity induced by immune checkpoint inhibitors: mechanisms linking immune dysregulation and myocardial fibrosis.American journal of clinical and experimental immunology · 2026Review
- 27-hydroxycholesterol and endothelial cell immune memory link maternal hypercholesterolemia with atherosclerosis in the offspring.Nature cardiovascular research · 2025Article
- CD248-targeted BBIR-T cell therapy against late-activated fibroblasts in cardiac repair after myocardial infarction.Nature communications · 2025Article
- Decoding cardiac metabolic reprogramming through single-cell multi-omics: from mechanisms to therapeutic applications.Frontiers in cell and developmental biology · 2025Review
- Potential Drug Targets and Causal Plasma Proteins Related to Preeclampsia Identified by Mendelian Randomization.Women's health reports (New Rochelle, N.Y.)Article
Corrections and comments
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Authors and funding
26 authors.
Funding
Abstract
Post-injury remodeling is a complex process involving temporal specific cellular interactions in the injured tissue where the resident fibroblasts play multiple roles. Here, we performed single-cell and spatial transcriptome analysis in human and mouse infarcted hearts to dissect the molecular basis of these interactions. We identified a unique fibroblast subset with high CD248 expression, strongly associated with extracellular matrix remodeling. Genetic Cd248 deletion in fibroblasts mitigated cardiac fibrosis and dysfunction following ischemia/reperfusion. Mechanistically, CD248 stabilizes type I transforming growth factor beta receptor and thus upregulates fibroblast ACKR3 expression, leading to enhanced T cell retention. This CD248-mediated fibroblast-T cell interaction is required to sustain fibroblast activation and scar expansion. Disrupting this interaction using monoclonal antibody or chimeric antigen receptor T cell reduces T cell infiltration and consequently ameliorates cardiac fibrosis and dysfunction. Our findings reveal a CD248
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