ReviewJournal of molecular and cellular cardiology2016
Mesenchymal stem cell-derived inflammatory fibroblasts mediate interstitial fibrosis in the aging heart.
Review in Journal of molecular and cellular cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 53 citations in OpenAlex.
- Cardiac fibroblast heterogeneity in cardiac fibrosis implication for cell-type-specific treatment.Frontiers in physiology · 2026Review
- Leptin as a key driver for organ fibrogenesis.Science advances · 2025Article
- Review
- Ferroptosis in diabetic cardiomyopathy: Advances in cardiac fibroblast-cardiomyocyte interactions.Heliyon · 2024Review
- Review
- The Senescent Heart-"Age Doth Wither Its Infinite Variety".International journal of molecular sciences · 2024Review
- A defective mechanosensing pathway affects fibroblast-to-myofibroblast transition in the old male mouse heart.iScience · 2023Article
- Expression profiles and functional analysis of tRNA-derived small RNAs in epicardial adipose tissue of patients with heart failure.Annals of medicine · 2023Article
- Aging of mesenchymal stem cell: machinery, markers, and strategies of fighting.Cellular & molecular biology letters · 2022Review
- Atypically Shaped Cardiomyocytes (ACMs): The Identification, Characterization and New Insights into a Subpopulation of Cardiomyocytes.Biomolecules · 2022Review
- Cardiac Mesenchymal Stem Cells Promote Fibrosis and Remodeling in Heart Failure: Role of PDGF Signaling.JACC. Basic to translational science · 2022Article
- Review
- Inhibition of lncRNAMolecular medicine reports · 2021Article
- Cardiac fibrosis.Cardiovascular research · 2021Review
- Article
- Sos1 Modulates Extracellular Matrix Synthesis, Proliferation, and Migration in Fibroblasts.Frontiers in physiology · 2021Article
- Ageing, sex, and cardioprotection.British journal of pharmacology · 2020Review
- Long-Lasting Anti-Inflammatory Activity of Human Microfragmented Adipose Tissue.Stem cells international · 2019Article
- Three in a Box: Understanding Cardiomyocyte, Fibroblast, and Innate Immune Cell Interactions to Orchestrate Cardiac Repair Processes.Frontiers in cardiovascular medicine · 2019Review
- Changes in cardiac resident fibroblast physiology and phenotype in aging.American journal of physiology. Heart and circulatory physiology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Pathologic fibrosis in the aging mouse heart is associated with dysregulated resident mesenchymal stem cells (MSC) arising from reduced stemness and aberrant differentiation into dysfunctional inflammatory fibroblasts. Fibroblasts derived from aging MSC secrete higher levels of 1) collagen type 1 (Col1) that directly contributes to fibrosis, 2) monocyte chemoattractant protein-1 (MCP-1) that attracts leukocytes from the blood and 3) interleukin-6 (IL-6) that facilitates transition of monocytes into myeloid fibroblasts. The transcriptional activation of these proteins is controlled via the farnesyltransferase (FTase)-Ras-Erk pathway. The intrinsic change in the MSC phenotype acquired by advanced age is specific for the heart since MSC originating from bone wall (BW-MSC) or fibroblasts derived from them were free of these defects. The potential therapeutic interventions other than clinically approved strategies based on findings presented in this review are discussed as well. This article is a part of a Special Issue entitled "Fibrosis and Myocardial Remodeling".
Indexed as
Identifiers
What OpenQuestion holds
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.