ArticleBasic research in cardiology2017
Dissecting the role of myeloid and mesenchymal fibroblasts in age-dependent cardiac fibrosis.
Article in Basic research in cardiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 35 citations in OpenAlex.
- The gene regulatory networks shaping macrophage plasticity and altered function in fibrosis.Frontiers in immunology · 2026Review
- Cellular Senescence, Inflammaging and Cardiovascular Disease.Immunological reviews · 2026Review
- Long-term dietary allyl isothiocyanate, a TRPA1 agonist, ameliorates cardiac fibrosis and diastolic dysfunction in aged mice.GeroScience · 2025Article
- Comparative phenotyping of C57BL/6J substrains reveals distinctive patterns of cardiac aging.GeroScience · 2025Article
- Sex Differences in Response to Diet Enriched With Glutathione Precursors in the Aging Heart.The journals of gerontology. Series A, Biological sciences and medical sciences · 2025Article
- Macrophages in organ fibrosis: from pathogenesis to therapeutic targets.Cell death discovery · 2024Review
- Macrophages in the infarcted heart acquire a fibrogenic phenotype, expressing matricellular proteins, but do not undergo fibroblast conversion.Journal of molecular and cellular cardiology · 2024Article
- Macrophages in cardiovascular diseases: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Mineralocorticoid receptor promotes cardiac macrophage inflammaging.Basic research in cardiology · 2024Article
- Polycystic Ovary Syndrome Fuels Cardiovascular Inflammation and Aggravates Ischemic Cardiac Injury.Circulation · 2023Article
- A defective mechanosensing pathway affects fibroblast-to-myofibroblast transition in the old male mouse heart.iScience · 2023Article
- Silencing of UTX Mitigates Aging-Associated Cardiac Fibrosis via Blocking Cardiac Fibroblasts-to-Myofibroblasts Trans-Differentiation.Anatolian journal of cardiology · 2023Article
- Ginaton reduces M1-polarized macrophages in hypertensive cardiac remodelingFrontiers in pharmacology · 2023Article
- Early Development of Cardiac Fibrosis in Young Old-Father Offspring.Oxidative medicine and cellular longevity · 2022Article
- Cardiac fibrosis.Cardiovascular research · 2021Review
- Treatment with a DC-SIGN ligand reduces macrophage polarization and diastolic dysfunction in the aging female but not male mouse hearts.GeroScience · 2021Article
- Fibrocytes: A Critical Review and Practical Guide.Frontiers in immunology · 2021Review
- Inflammatory Cytokines and Chemokines as Therapeutic Targets in Heart Failure.Cardiovascular drugs and therapy · 2020Review
- Mechanosensing dysregulation in the fibroblast: A hallmark of the aging heart.Ageing research reviews · 2020Review
- Leucocyte count predicts cardiovascular risk in heart failure with preserved ejection fraction: insights from TOPCAT Americas.ESC heart failure · 2020Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Aging is associated with increased cardiac interstitial fibrosis and diastolic dysfunction. Our previous study has shown that mesenchymal fibroblasts in the C57BL/6J (B6J) aging mouse heart acquire an inflammatory phenotype and produce higher levels of chemokines. Monocyte chemoattractant protein-1 (MCP-1) secreted by these aged fibroblasts promotes leukocyte uptake into the heart. Some of the monocytes that migrate into the heart polarize into M2a macrophages/myeloid fibroblasts. The number of activated mesenchymal fibroblasts also increases with age, and consequently, both sources of fibroblasts contribute to fibrosis. Here, we further investigate mechanisms by which inflammation influences activation of myeloid and mesenchymal fibroblasts and their collagen synthesis. We examined cardiac fibrosis and heart function in three aged mouse strains; we compared C57BL/6J (B6J) with two other strains that have reduced inflammation via different mechanisms. Aged C57BL/6N (B6N) hearts are protected from oxidative stress and fibroblasts derived from them do not develop an inflammatory phenotype. Likewise, these mice have preserved diastolic function. Aged MCP-1 null mice on the B6J background (MCP-1KO) are protected from elevated leukocyte infiltration; they develop moderate but reduced fibrosis and diastolic dysfunction. Based on these studies, we further delineated the role of resident versus monocyte-derived M2a macrophages in myeloid-dependent fibrosis and found that the number of monocyte-derived M2a (but not resident) macrophages correlates with age-related fibrosis and diastolic dysfunction. In conclusion, we have found that ROS and inflammatory mediators are necessary for activation of fibroblasts of both developmental origins, and prevention of either led to better functional outcomes.
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