ArticleF1000Research2013
Tissue-resident Sca1+ PDGFRα+ mesenchymal progenitors are the cellular source of fibrofatty infiltration in arrhythmogenic cardiomyopathy.
Article in F1000Research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Fibroblast-Specific Loss of TGF-β Signaling Mediates Lipomatous Metaplasia in the Infarcted Heart.Circulation · 2025Article
- Review
- Prx1 + and Hic1+ Mesenchymal Progenitors Are Present Within the Epidural Fat and Dura Mater and Participate in Dural Injury Repair.Stem cells translational medicine · 2022Article
- Partial Ablation of Non-Myogenic Progenitor Cells as a Therapeutic Approach to Duchenne Muscular Dystrophy.Biomolecules · 2021Article
- Tissue-Resident PDGFRαCell reports · 2020Article
- The interstitium in cardiac repair: role of the immune-stromal cell interplay.Nature reviews. Cardiology · 2018Review
- Sca-1European journal of immunology · 2018Article
- Arrhythmogenic Cardiomyopathy: the Guilty Party in Adipogenesis.Journal of cardiovascular translational research · 2017Review
- Prolactin mediates effects of chronic psychological stress on induction of fibrofatty cells in the heart.American journal of translational research · 2016Article
- Pathological Left Ventricular Hypertrophy and Stem Cells: Current Evidence and New Perspectives.Stem cells international · 2016Review
- Sca-1+ cardiac progenitor cells and heart-making: a critical synopsis.Stem cells and development · 2014Review
- Cardiogenic genes expressed in cardiac fibroblasts contribute to heart development and repair.Circulation research · 2014Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Arrhythmogenic cardiomyopathy (AC) is a disease of the heart involving myocardial dystrophy leading to fibrofatty scarring of the myocardium and is associated with an increased risk of both ventricular arrhythmias and sudden cardiac death. It often affects the right ventricle but may also involve the left. Although there has been significant progress in understanding the role of underlying desmosomal genetic defects in AC, there is still a lack of data regarding the cellular processes involved in its progression. The development of cardiac fibrofatty scarring is known to be a principal pathological process associated with ventricular arrhythmias, and it is vital that we elucidate the role of various cell populations involved in the disease if targeted therapeutics are to be developed. The known role of mesenchymal progenitor cells in the reparative process of both the heart and skeletal muscle has provided inspiration for the identification of the cellular basis of fibrofatty infiltration in AC. Here we hypothesize that reparative processes triggered by myocardial degeneration lead to the differentiation of tissue-resident Sca1+ PDGFRα+ mesenchymal progenitors into adipocytes and fibroblasts, which compose the fibrofatty lesions characteristic of AC.
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Registered trials
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.