Mast Cells in Cardiac Fibrosis: New Insights Suggest Opportunities for Intervention
Open accessAbstract
Mast cells (MC) are innate immune cells present in virtually all body tissues with key roles in allergic disease and host defense. MCs recognize damage-associated molecular patterns (DAMPs) through expression of multiple receptors including Toll-like receptors and the IL-33 receptor ST2. MCs can be activated to degranulate and release pre-formed mediators, to synthesize and secrete cytokines and chemokines without degranulation, and/or to produce lipid mediators. MC numbers are generally increased at sites of fibrosis. They are potent, resident, effector cells producing mediators that regulate the fibrotic process. The nature of the secretory products produced by MCs depend on micro-environmental signals and can be both pro- and anti-fibrotic. MCs have been repeatedly implicated in the pathogenesis of cardiac fibrosis and in angiogenic responses in hypoxic tissues, but these findings are controversial. Several rodent studies have indicated a protective role for MCs. MC-deficient mice have been reported to have poorer outcomes after coronary artery ligation and increased cardiac function upon MC reconstitution. In contrast, MCs have also been implicated as key drivers of fibrosis. MC stabilization during a hypertensive rat model and an atrial fibrillation mouse model rescued associated fibrosis. Discrepancies in the literature could be related to problems with mouse models of MC deficiency. To further complicate the issue, mice generally have a much lower density of MCs in their cardiac tissue than humans, and as such comparing MC deficient and MC containing mouse models is not necessarily reflective of the role of MCs in human disease. In this review, we will evaluate the literature regarding the role of MCs in cardiac fibrosis with an emphasis on what is known about MC biology, in this context. MCs have been well-studied in allergic disease and multiple pharmacological tools are available to regulate their function. We will identify potential opportunities to manipulate human MC function and the impact of their mediators with a view to preventing or reducing harmful fibrosis. Important therapeutic opportunities could arise from increased understanding of the impact of such potent, resident immune cells, with the ability to profoundly alter long term fibrotic processes.
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Resident mast cells are found in tissues such as the heart in small numbers, and they are highly potent with local and far-ranging effects that influence the immune, hormone (including sex hormones), and central/peripheral nervous systems.
“Although resident mast cells are found in tissues such as the heart in small numbers, they are highly potent with local and far-ranging effects that influence the immune, hormone (including sex hormones), and central/peripheral nervous systems (Figure 4). 171”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [171]
The Introduction describes mast cells as tissue-resident cells found in the heart and as potent regulators of immune responses; the Confounding Factors section reports low cardiac mast-cell density specifically in mice, not across tissues or species. The paper does not establish the claimed far-ranging effects on hormone systems, including sex hormones, or on the central and peripheral nervous systems. (LLM, conf=0.87)
Experimental — accuracy not yet measuredMast cells are critical for the remodeling and fibrosis that lead to DCM, due to their release of profibrotic cytokines (eg, IL-1β, TGFβ1, and TNFα) and enzymes including Serpin A3n that are required to activate IL-1β and matrix metalloproteinases required for fibrosis.
“Mast cells are critical for the remodeling and fibrosis that lead to DCM, due to their release of profibrotic cytokines (eg, IL-1 β , TGF β 1 [transforming growth factor beta 1], and TNF α ), and many enzymes, including Serpin A3n ( α 1-antichymotrypsin), that are required to activate IL-1 β and matrix metalloproteinases that are required for fibrosis (Figure 4). 129,171”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [171]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredMast cells have a wide array of roles including as APCs that respond to infections.
“Although mast cells are typically associated with IgEmediated allergic responses, they have a wide array of roles including as APCs that respond to infections (Figure 4). 171”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [171]
The Introduction describes mast cells as multifunctional sentinel cells that detect pathogen-associated signals and says their degranulation contributes to inflammatory processes in infection. It does not identify them as antigen-presenting cells (APCs), so that specific role is not supported by our copy. (LLM, conf=0.85)
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- Authors
- Legere, S. A., Haidl, I. D., Légaré, J.-F., & Marshall, J. S.
- Affiliations
- Dalhousie University (CA)
- Corresponding author
- Marshall, Jean S.
- Venue
- Frontiers in Immunology
- Publisher
- Frontiers Media SA
- Published
- 2019-03-28
- Volume
- 10
- Pages
- 580-580
- ISSN
- 1664-3224 (ISSN-L)
- PMC
- PMC6455071
- OpenAlex
- W2919852644
- Cited by
- 92
- References
- 132
- Citations by year
- 2026: 8 · 2025: 11 · 2024: 14 · 2023: 11 · 2022: 12 · 2021: 15 · 2020: 18 · 2019: 2
- FWCI
- 2.13
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Immunology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Heart and Stroke Foundation of Canada
- Dalhousie Medical Research Foundation (394140)
- Dalhousie University
- Killam Trusts
- Canadian Institutes of Health Research (394140, THC135230, 135230)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Life Sciences › Immunology and Microbiology › Immunology › Mast cells and histamine
- Health Sciences › Medicine › Genetics › Mesenchymal stem cell research
- Keywords
- mast cells, myocardial fibrosis, mast cell degranulation, damage-associated molecular patterns, ST2, Toll-like receptors, mast cell stabilizers, mast cell-deficient mice, coronary artery ligation, atrial fibrillation, hypertension, angiogenesis, therapeutic target
- MeSH terms
- Interleukin-33, Interleukin-1 Receptor-Like 1 Protein, Animals, Fibrosis, Humans, Immunity, Innate, Mast Cells, Neovascularization, Pathologic, Rats, Inbred SHR, Myocardial Ischemia, Toll-Like Receptors, Mice, Rats
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