ArticleJournal of molecular and cellular cardiology2013
Coronary adventitial cells are linked to perivascular cardiac fibrosis via TGFβ1 signaling in the mdx mouse model of Duchenne muscular dystrophy.
Article in Journal of molecular and cellular cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 55 citations in OpenAlex.
- Effects of arginine vasopressin deficiency on cardiac fibrosis in male Wistar rats.Physiological reports · 2026Article
- Inhibition of miR-25 ameliorates cardiac and skeletal muscle dysfunction in agedMolecular therapy. Nucleic acids · 2024Article
- Mural cells interact with macrophages in the dura mater to regulate CNS immune surveillance.The Journal of experimental medicine · 2024Article
- Novel implementation of cardiac magnetic resonance first-pass perfusion imaging for semi-quantitatively evaluating microvascular dysfunction in paediatric patients with Duchenne muscular dystrophy.The British journal of radiology · 2024Article
- The Protective Effects of γ-Tocotrienol on Muscle Stem Cells Through Inhibiting Reactive Oxidative Stress Production.Frontiers in cell and developmental biology · 2022Article
- Complexity of skeletal muscle degeneration: multi-systems pathophysiology and organ crosstalk in dystrophinopathy.Pflugers Archiv : European journal of physiology · 2021Review
- Review
- Therapeutic aspects of cell signaling and communication in Duchenne muscular dystrophy.Cellular and molecular life sciences : CMLS · 2021Review
- Cardiac fibrosis.Cardiovascular research · 2021Review
- Aortic carboxypeptidase-like protein regulates vascular adventitial progenitor and fibroblast differentiation through myocardin related transcription factor A.Scientific reports · 2021Article
- Distinct Fibroblast Lineages Give Rise to NG2+ Pericyte Populations in Mouse Skin Development and Repair.Frontiers in cell and developmental biology · 2021Article
- Evolving Roles of Muscle-Resident Fibro-Adipogenic Progenitors in Health, Regeneration, Neuromuscular Disorders, and Aging.Frontiers in physiology · 2021Review
- Role of the Renin-Angiotensin-Aldosterone System in Dystrophin-Deficient Cardiomyopathy.International journal of molecular sciences · 2020Review
- Smooth muscle-derived progenitor cell myofibroblast differentiation through KLF4 downregulation promotes arterial remodeling and fibrosis.JCI insight · 2020Article
- The orphan nuclear receptor Nr4a1 mediates perinatal neuroinflammation in a murine model of preterm labor.Cell death & disease · 2020Article
- Role of Metabolic Stress and Exercise in Regulating Fibro/Adipogenic Progenitors.Frontiers in cell and developmental biology · 2020Review
- Nintedanib decreases muscle fibrosis and improves muscle function in a murine model of dystrophinopathy.Cell death & disease · 2018Article
- Rosmarinic acid attenuates cardiac fibrosis following long-term pressure overload via AMPKα/Smad3 signaling.Cell death & disease · 2018Article
- Tracking Adventitial Fibroblast Contribution to Disease: A Review of Current Methods to Identify Resident Fibroblasts.Arteriosclerosis, thrombosis, and vascular biology · 2017Review
- Redefining the identity of cardiac fibroblasts.Nature reviews. Cardiology · 2017Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
In Duchenne muscular dystrophy (DMD), progressive accumulation of cardiac fibrosis promotes heart failure. While the cellular origins of fibrosis in DMD hearts remain enigmatic, fibrotic tissue conspicuously forms near the coronary adventitia. Therefore, we sought to characterize the role of coronary adventitial cells in the formation of perivascular fibrosis. Utilizing the mdx model of DMD, we have identified a population of Sca1+, PDGFRα+, CD31-, and CD45- coronary adventitial cells responsible for perivascular fibrosis. Histopathology of dystrophic hearts revealed that Sca1+ cells extend from the adventitia and occupy regions of perivascular fibrosis. The number of Sca1+ adventitial cells increased two-fold in fibrotic mdx hearts vs. age matched wild-type hearts. Moreover, relative to Sca1-, PDGFRα+, CD31-, and CD45- cells and endothelial cells, Sca1+ adventitial cells FACS-sorted from mdx hearts expressed the highest level of Collagen1α1 and 3α1, Connective tissue growth factor, and Tgfβr1 transcripts. Surprisingly, mdx endothelial cells expressed the greatest level of the Tgfβ1 ligand. Utilizing Collagen1α1-GFP reporter mice, we confirmed that the majority of Sca1+ adventitial cells expressed type I collagen, an abundant component of cardiac fibrosis, in both wt (71%±4.1) and mdx (77%±3.5) hearts. In contrast, GFP+ interstitial fibroblasts were PDGFRα+ but negative for Sca1. Treatment of cultured Collagen1α1-GFP+ adventitial cells with TGFβ1 resulted in increased collagen synthesis, whereas pharmacological inhibition of TGFβR1 signaling reduced the fibrotic response. Therefore, perivascular cardiac fibrosis by coronary adventitial cells may be mediated by TGFβ1 signaling. Our results implicate coronary endothelial cells in mediating cardiac fibrosis via transmural TGFβ signaling, and suggest that the coronary adventitia is a promising target for developing novel anti-fibrotic therapies.
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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.