ReviewJournal of molecular and cellular cardiology2014
Adverse fibrosis in the aging heart depends on signaling between myeloid and mesenchymal cells; role of inflammatory fibroblasts.
Review in Journal of molecular and cellular cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
36 citing papers in PubMed, 57 citations in OpenAlex.
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- Secular trend in disease burden of atrial fibrillation/flutter in China from 1992 to 2021 and its projection in 25 years.BMC public health · 2025Article
- The Senescent Heart-"Age Doth Wither Its Infinite Variety".International journal of molecular sciences · 2024Review
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- Cardiovascular aging: from cellular and molecular changes to therapeutic interventions.The journal of cardiovascular aging · 2023Article
- Transforming growth factor-β in myocardial disease.Nature reviews. Cardiology · 2022Review
- Clinical Skin Aging Score and Risk of Degenerative Cardiovascular Diseases.The Journal of clinical and aesthetic dermatology · 2021Article
- Mechanosensing dysregulation in the fibroblast: A hallmark of the aging heart.Ageing research reviews · 2020Review
- Predicting and Promoting Human Bone Marrow MSC Chondrogenesis by Way of TGFβ Receptor Profiles: Toward Personalized Medicine.Frontiers in bioengineering and biotechnology · 2020Article
- Low-Dose Pesticide Mixture Induces Accelerated Mesenchymal Stem Cell Aging In Vitro.Stem cells (Dayton, Ohio) · 2019Article
- Single-Cell Transcriptomics of Human Mesenchymal Stem Cells Reveal Age-Related Cellular Subpopulation Depletion and Impaired Regenerative Function.Stem cells (Dayton, Ohio) · 2019Article
- Biomarkers for the identification of cardiac fibroblast and myofibroblast cells.Heart failure reviews · 2019Review
- Novel role of extracellular matrix protein 1 (ECM1) in cardiac aging and myocardial infarction.PloS one · 2019Article
- Changes in cardiac resident fibroblast physiology and phenotype in aging.American journal of physiology. Heart and circulatory physiology · 2018Review
- Improved Cardiovascular Function in Old Mice After N-Acetyl Cysteine and Glycine Supplemented Diet: Inflammation and Mitochondrial Factors.The journals of gerontology. Series A, Biological sciences and medical sciences · 2018Article
- Sirtuins and Accelerated Aging in Scleroderma.Current rheumatology reports · 2018Review
- The allosteric glycogen synthase kinase-3 inhibitor NP12 limits myocardial remodeling and promotes angiogenesis in an acute myocardial infarction model.The Journal of biological chemistry · 2017Article
- Aicar treatment reduces interstitial fibrosis in aging mice: Suppression of the inflammatory fibroblast.Journal of molecular and cellular cardiology · 2017Article
- Dissecting the role of myeloid and mesenchymal fibroblasts in age-dependent cardiac fibrosis.Basic research in cardiology · 2017Article
- Influences of age-related changes in mesenchymal stem cells on macrophages during in-vitro culture.Stem cell research & therapy · 2017Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Aging has been associated with adverse fibrosis. Here we formulate a new hypothesis and present new evidence that unresponsiveness of mesenchymal stem cells (MSC) and fibroblasts to transforming growth factor beta (TGF-β), due to reduced expression of TGF-β receptor I (TβRI), provides a foundation for cardiac fibrosis in the aging heart via two mechanisms. 1) TGF-β promotes expression of Nanog, a transcription factor that retains MSC in a primitive state. In MSC derived from the aging heart, Nanog expression is reduced and therefore MSC gradually differentiate and the number of mesenchymal fibroblasts expressing collagen increases. 2) As TGF-β signaling pathway components negatively regulate transcription of monocyte chemoattractant protein-1 (MCP-1), a reduced expression of TβRI prevents aging mesenchymal cells from shutting down their own MCP-1 expression. Elevated MCP-1 levels that originated from MSC attract transendothelial migration of mononuclear leukocytes from blood to the tissue. MCP-1 expressed by mesenchymal fibroblasts promotes further migration of monocytes and T lymphocytes away from the endothelial barrier and supports the monocyte transition into macrophages and finally into myeloid fibroblasts. Both myeloid and mesenchymal fibroblasts contribute to fibrosis in the aging heart via collagen synthesis. This article is part of a Special Issue entitled "Myocyte-Fibroblast Signalling in Myocardium ".
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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.