ArticleCommunications biology2023
IL-1β-mediated adaptive reprogramming of endogenous human cardiac fibroblasts to cells with immune features during fibrotic remodeling.
Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Macrophage-Dependent Intercellular Crosstalk in Multiphenotypic Heart Failure With Preserved Ejection Fraction.Journal of the American Heart Association · 2026Review
- Molecular imaging of immune and fibrosis targets to guide therapy for repair after myocardial infarction.Nature reviews. Cardiology · 2026Review
- PHLDA1 is a shared diagnostic and key mediator of inflammatory fibrosis in heart and kidney.Frontiers in immunology · 2026Article
- Canonical and emerging regulatory mechanisms of tissue remodeling: shared principles across organs and therapeutic opportunities.Frontiers in immunology · 2026Review
- Berberine suppresses colon inflammation via integrated modulation of host metabolism, microbial ecology, and innate immune signaling.Theranostics · 2026Article
- TET3 is a regulator and can be targeted for the intervention of myocardial fibrosis.EMBO molecular medicine · 2025Article
- Early immune response toMicrobiology spectrum · 2025Article
- Unexpectedly High and Difficult-to-Explain Regenerative Capacity in an 82-Year-Old Patient with Insulin-Requiring Type 2 Diabetes and End-Stage Renal Disease.Journal of clinical medicine · 2025Article
- The epigenetic regulation of crosstalk between cardiac fibroblasts and other cardiac cell types during stress.Frontiers in cardiovascular medicine · 2025Review
- Article
- Cardiac Fibroblastic Niches in Homeostasis and Inflammation.Circulation research · 2024Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
Abstract
The source and roles of fibroblasts and T-cells during maladaptive remodeling and myocardial fibrosis in the setting of pulmonary arterial hypertension (PAH) have been long debated. We demonstrate, using single-cell mass cytometry, a subpopulation of endogenous human cardiac fibroblasts expressing increased levels of CD4, a helper T-cell marker, in addition to myofibroblast markers distributed in human fibrotic RV tissue, interstitial and perivascular lesions in SUGEN/Hypoxia (SuHx) rats, and fibroblasts labeled with pdgfrα CreERt2/+ in R26R-tdTomato mice. Recombinant IL-1β increases IL-1R, CCR2 receptor expression, modifies the secretome, and differentiates cardiac fibroblasts to form CD68-positive cell clusters. IL-1β also activates stemness markers, such as NANOG and SOX2, and genes involved in dedifferentiation, lymphoid cell function and metabolic reprogramming. IL-1β induction of lineage traced primary mouse cardiac fibroblasts causes these cells to lose their fibroblast identity and acquire an immune phenotype. Our results identify IL-1β induced immune-competency in human cardiac fibroblasts and suggest that fibroblast secretome modulation may constitute a therapeutic approach to PAH and other diseases typified by inflammation and fibrotic remodeling.
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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.