Gata6+ Pericardial Cavity Macrophages Relocate to the Injured Heart and Prevent Cardiac Fibrosis
Open accessAbstract
Macrophages play an important role in structural cardiac remodeling and the transition to heart failure following myocardial infarction (MI). Previous research has focused on the impact of blood-derived monocytes on cardiac repair. Here we examined the contribution of resident cavity macrophages located in the pericardial space adjacent to the site of injury. We found that disruption of the pericardial cavity accelerated maladaptive post-MI cardiac remodeling. Gata6+ macrophages in mouse pericardial fluid contributed to the reparative immune response. Following experimental MI, these macrophages invaded the epicardium and lost Gata6 expression but continued to perform anti-fibrotic functions. Loss of this specialized macrophage population enhanced interstitial fibrosis after ischemic injury. Gata6+ macrophages were present in human pericardial fluid, supporting the notion that this reparative function is relevant in human disease. Our findings uncover an immune cardioprotective role for the pericardial tissue compartment and argue for the reevaluation of surgical procedures that remove the pericardium.
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The αv-containing integrins αvβ1, αvβ3, αvβ5, αvβ6, and αvβ8 bind to the latency-associated peptide (LAP) of TGF-β1.
“the integrins αvβ1, αvβ3, αvβ5, αvβ6 and αvβ8 have all been shown to bind to an N-terminal fragment of the TGFβ1 gene product called the latency associated peptide (LAP)”
From Fibrosis: from mechanisms to medicines (2020) · cites this paper as [89]
LAP normally forms a noncovalent latent complex with active TGF-β, preventing TGF-β from binding its receptors and inducing biological effects.
“which normally forms a noncovalent complex (latent complex) with the active cytokine, preventing TGF-β from binding to its cognate receptors and inducing biological effects89–93”
From Fibrosis: from mechanisms to medicines (2020) · cites this paper as [89]
Small molecule inhibitors of αvβ1 have an anti-fibrotic effect in models of lung and liver fibrosis.
“recent studies demonstrating an anti-fibrotic effect of αvβ1 blockade in models of lung and liver fibrosis89”
From Fibrosis: from mechanisms to medicines (2020) · cites this paper as [89]
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- Authors
- Deniset, J. F., Belke, D., Lee, W.-Y., Jorch, S. K., Deppermann, C., Hassanabad, A. F., Turnbull, J. D., Teng, G., Rozich, I., Hudspeth, K., Kanno, Y., Brooks, S. R., Hadjantonakis, A.-K., O’Shea, J. J., Weber, G. F., Fedak, P. W. M., & Kubes, P.
- Affiliations
- University of Calgary (CA)
- National Institutes of Health (US)
- Memorial Sloan Kettering Cancer Center (US)
- Friedrich-Alexander-Universität Erlangen-Nürnberg (DE)
- Corresponding author
- Kubes, Paul
- ORCID
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2019-07
- Volume
- 51
- Issue
- 1
- Pages
- 131-140.e5
- ISSN
- 1074-7613 (ISSN-L)
- PMC
- PMC7574643
- OpenAlex
- W2961520678
- Cited by
- 178
- References
- 27
- Citations by year
- 2026: 21 · 2025: 25 · 2024: 28 · 2023: 22 · 2022: 19 · 2021: 32 · 2020: 26 · 2019: 5
- FWCI
- 14.81
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Heart and Stroke Foundation of Canada (G-18-0020471)
- 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 › Genetics › Mesenchymal stem cell research
- Keywords
- myocardial infarction, myocardial fibrosis, cardiac remodeling, pericardial fluid, pericardial surgery, myocardial ischemic injury
- MeSH terms
- Animals, Cell Movement, Cells, Cultured, Fibrosis, Heart, Humans, Macrophages, Mice, Inbred C57BL, Mice, Transgenic, Myocardial Infarction, Myocardium, Pericardium, Ventricular Remodeling, GATA6 Transcription Factor, Mice
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