Sca‐1 + cardiac fibroblasts promote development of heart failure
Open accessAbstract
The causative effect of GM‐CSF produced by cardiac fibroblasts to development of heart failure has not been shown. We identified the pathological GM‐CSF‐producing cardiac fibroblast subset and the specific deletion of IL‐17A signaling to these cells attenuated cardiac inflammation and heart failure. We describe here the CD45 − CD31 − CD29 + mEF‐SK4 + PDGFRα + Sca‐1 + periostin + (Sca‐1 + ) cardiac fibroblast subset as the main GM‐CSF producer in both experimental autoimmune myocarditis and myocardial infarction mouse models. Specific ablation of IL‐17A signaling to Sca‐1 + periostin + cardiac fibroblasts ( Postn Cre Il17ra fl/fl ) protected mice from post‐infarct heart failure and death. Moreover, Postn Cre Il17ra fl/fl mice had significantly fewer GM‐CSF‐producing Sca‐1 + cardiac fibroblasts and inflammatory Ly6C hi monocytes in the heart. Sca‐1 + cardiac fibroblasts were not only potent GM‐CSF producers, but also exhibited plasticity and switched their cytokine production profiles depending on local microenvironments. Moreover, we also found GM‐CSF‐positive cardiac fibroblasts in cardiac biopsy samples from heart failure patients of myocarditis or ischemic origin. Thus, this is the first identification of a pathological GM‐CSF‐producing cardiac fibroblast subset in human and mice hearts with myocarditis and ischemic cardiomyopathy. Sca‐1 + cardiac fibroblasts direct the type of immune cells infiltrating the heart during cardiac inflammation and drive the development of heart failure.
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This signalling, amplified by macrophage-derived cytokines such as IL-1β and TNF-α, transforms cardiac fibroblasts into active immune-like inflammatory hubs secreting CSF2 and CCL2.
“This signalling, amplified by macrophage-derived cytokines such as IL-1β and TNF-α, transforms cardiac fibroblasts into active immune-like inflammatory hubs secreting CSF2 and CCL2 [13,14].”
From Cardiac Macrophages Exhibit Dynamic Heterogeneity and Functional Specialization During Experimental Autoimmune Myocarditis. (2026) · cites this paper as [13]
The Results section (page not provided) reports that Sca-1+ cardiac fibroblasts express Csf2 and Ccl2 in response to IL-17A, and that TNF-α can synergize with IL-17A. The cited passages do not establish that the TNF-α is macrophage-derived or that IL-1β amplifies this response. (LLM, conf=0.87)
Experimental — accuracy not yet measuredDuring the acute inflammatory phase of EAM, elevated levels of interleukin-17A stimulate extensive cardiac fibrosis and irregular collagen deposition.
“During the acute inflammatory phase of EAM, elevated levels of interleukin-17A stimulate extensive cardiac fibrosis and irregular collagen deposition [8,10,13].”
From Cardiac Macrophages Exhibit Dynamic Heterogeneity and Functional Specialization During Experimental Autoimmune Myocarditis. (2026) · cites this paper as [13]
The Introduction says IL-17A signaling to cardiac fibroblasts contributes to heart-failure development in EAM, and the Results report IL-17A-dependent fibroblast activity during cardiac inflammation (day 21). The cited passages do not establish elevated IL-17A levels during the acute phase or show that IL-17A causes extensive fibrosis and irregular collagen deposition in EAM. No page numbers are available in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredWithin these niches, macrophage-dependent signalling pathways drive adverse remodelling through intense crosstalk with cardiac fibroblasts.
“Within these niches, macrophage-dependent signalling pathways drive adverse remodelling through intense crosstalk with cardiac fibroblasts [13].”
From Cardiac Macrophages Exhibit Dynamic Heterogeneity and Functional Specialization During Experimental Autoimmune Myocarditis. (2026) · cites this paper as [13]
The Introduction and Discussion describe signalling between cardiac fibroblasts and immune cells that contributes to heart failure. But they identify IL-17A signalling to fibroblasts and fibroblast-driven recruitment of inflammatory monocytes, not macrophage-dependent signalling that drives adverse remodelling. Page numbers are unavailable in our copy. (LLM, conf=0.83)
Experimental — accuracy not yet measuredIL-17A-driven inflammation synergizes with macrophage-derived signals to promote maladaptive remodelling.
“This is consistent with previous findings demonstrating that IL-17A-driven inflammation synergizes with macrophage-derived signals to promote maladaptive remodelling [10,13].”
From Cardiac Macrophages Exhibit Dynamic Heterogeneity and Functional Specialization During Experimental Autoimmune Myocarditis. (2026) · cites this paper as [13]
The Results section on IL-17RA ablation reports that blocking IL-17A signaling in cardiac fibroblasts reduced inflammatory monocytes and infarct size and improved post-MI survival. The paper also reports synergy between TNF-α and IL-17A in fibroblast gene production, but it does not identify the synergizing signal as macrophage-derived or demonstrate that macrophage-derived signals synergize with IL-17A to drive remodelling. No page numbers were available in our copy. (LLM, conf=0.86)
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Fibroblast Primary Cilia Are Required for Cardiac Fibrosis
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Macrophages in Heart Failure with Reduced versus Preserved Ejection Fraction
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The Cardiac Microenvironment Instructs Divergent Monocyte Fates and Functions in Myocarditis
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Self-citationGrowth Factors as Immunotherapeutic Targets in Cardiovascular Disease
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Autoimmune Myocarditis, Old Dogs and New Tricks.
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Self-citationNon-cytotoxic Cardiac Innate Lymphoid Cells Are a Resident and Quiescent Type 2-Commited Population
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Innate Lymphoid Cells Play a Pathogenic Role in Pericarditis
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Effect of injection of different doses of isoproterenol on the hearts of mice
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Multilineage contribution of CD34+ cells in cardiac remodeling after ischemia/reperfusion injury
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Myocarditis and carotidynia caused by Granulocyte-Colony stimulating factor administration
de la Fuente, E. C., Barquín, A., Saavedra, C., Domingo, J. J. S., Huertas, R. M., Fernández-Abad, M., & Martínez-Jáñez, N. (2020) · Modern Rheumatology Case Reports · doi:10.1080/24725625.2020.1754552 · Cited by 9 · see citing works
Hypereosinophilia causes progressive cardiac pathologies in mice
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Fibroblast-Specific Loss of TGF-β Signaling Mediates Lipomatous Metaplasia in the Infarcted Heart
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Pdgfrα+ stromal cells, a key regulator for tissue homeostasis and dysfunction in distinct organs
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Myocardial Immune Niches in Homeostasis and Inflammation
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“This is consistent with previous findings demonstrating that IL-17A-driven inflammation synergizes with macrophage-derived signals to promote maladaptive remodelling [10,13].”
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Additional file 1 of Effect of injection of different doses of isoproterenol on the hearts of mice
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IL-1–Activated Inflammatory Cardiac Fibroblasts Exacerbate Acute Coxsackievirus B3 Myocarditis
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Inflammatory Fibroblasts Ready for Their Close-up
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- Authors
- Chen, G., Bracamonte‐Baran, W., Diny, N. L., Hou, X., Talor, M. V., Fu, K., Liu, Y., Davogustto, G., Vasquez, H., Taegtmeyer, H., Frazier, O. H., Waisman, A., Conway, S. J., Wan, F., & Čiháková, D.
- Affiliations
- Johns Hopkins University (US)
- The University of Texas Health Science Center at Houston (US)
- Texas Heart Institute CHI St. Luke's Health ‐ Baylor St. Luke's Medical Center MC 2–114A PO Box 20345 Houston TX USA
- Johannes Gutenberg University Mainz (DE)
- Indiana University Indianapolis (US)
- Corresponding author
- Čiháková, Daniela
- ORCID
- Venue
- European Journal of Immunology
- Publisher
- Wiley
- Published
- 2018-07-18
- Volume
- 48
- Issue
- 9
- Pages
- 1522-1538
- ISSN
- 0014-2980 (ISSN-L)
- 1521-4141
- PMC
- PMC6696927
- OpenAlex
- W2811050705
- Cited by
- 53
- References
- 85
- Citations by year
- 2026: 6 · 2025: 3 · 2024: 6 · 2023: 4 · 2022: 8 · 2021: 3 · 2020: 12 · 2019: 9 · 2018: 2
- FWCI
- 4.92
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- European Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- IUScholarWorks (Indiana University) (submittedVersion)
- Purdue University Indianapolis (Indiana University) (submittedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01HL118183, R01HL136586)
- Myocarditis Foundation (90072351)
- Johns Hopkins Bloomberg School of Public Health
- National Institute of General Medical Sciences (R01GM111682)
- American Heart Association (16POST31330012, 17GRNT33700274)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Viral Infections and Immunology Research
- Keywords
- heart failure, GM-CSF, IL-17A signaling, periostin, cardiac inflammation, experimental autoimmune myocarditis, myocardial infarction, ischemic cardiomyopathy, Ly6C+ monocytes, fibroblast plasticity
- MeSH terms
- Ataxin-1, Animals, Cells, Cultured, Fibroblasts, Heart Failure, Humans, Mice, Inbred BALB C, Mice, Inbred C57BL, Myocardial Infarction, Myocarditis, Granulocyte-Macrophage Colony-Stimulating Factor, Mice, Knockout, Chemokine CCL2, Interleukin-17, Myocytes, Cardiac, Mice
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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