ReviewFrontiers in molecular biosciences2021
Modulation of Cardiac Fibrosis in and Beyond Cells.
Review in Frontiers in molecular biosciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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.
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Who cites it
19 citing papers in PubMed.
- From Ischemic Injury to Arrhythmogenic Substrate: Molecular and Histopathological Insights into Post-Infarction Sudden Cardiac Death.Life (Basel, Switzerland) · 2026Review
- Bioinformatics Identification and Molecular Docking Validation of Post-Translational Modification-Related Hub Genes as Diagnostic Biomarkers and Therapeutic Targets in Myocardial Fibrosis.International journal of molecular sciences · 2026Article
- 3D bioprinting of microfluidic systems for cardiac regenerative medicine: from biofabrication to organ-on-a-chip.Journal of biological engineering · 2026Review
- Article
- Non-invasive Evaluation of Myocardial Fibrosis Using T1 and T2 Mapping by Cardiac Magnetic Resonance Imaging.Cureus · 2026Review
- Therapeutic Targets for Myocardial Fibrosis: A Comprehensive Review of Current and Emerging Approaches.Cardiovascular & hematological disorders drug targets · 2026Review
- The Role of MCPIP1 in Macrophage Polarization and Cardiac Function Post-Myocardial Infarction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Sex-dependent Pathophysiology and Therapeutic Considerations in Right Heart Disease.The Canadian journal of cardiology · 2025Review
- Exosomal miR-15a-5p from cardiomyocytes promotes myocardial fibrosis.Molecular and cellular biochemistry · 2025Article
- Gene expression profiles, potential targets and treatments of cardiac remodeling.Molecular and cellular biochemistry · 2025Review
- An overview of the multi-dimensional mechanisms of exercise-regulated hormones and growth factors in cardiac physiological adaptation.Frontiers in physiology · 2025Review
- Inhibition of tartrate-resistant acid phosphatase 5 can prevent cardiac fibrosis after myocardial infarction.Molecular medicine (Cambridge, Mass.) · 2024Article
- Swimming alleviates myocardial fibrosis of type II diabetic rats through activating miR-34a-mediated SIRT1/PGC-1α/FNDC5 signal pathway.PloS one · 2024Article
- FIGNL1 Promotes Hepatocellular Carcinoma FormationCurrent gene therapy · 2024Article
- In-depth analysis of lupeol: delving into the diverse pharmacological profile.Frontiers in pharmacology · 2024Review
- The role of SMAD signaling in hypertrophic obstructive cardiomyopathy: an immunohistopathological study in pediatric and adult patients.Scientific reports · 2023Article
- Interferon-β decreases LPS-induced neutrophil recruitment to cardiac fibroblasts.Frontiers in cell and developmental biology · 2023Article
- Signaling pathways and targeted therapy for myocardial infarction.Signal transduction and targeted therapy · 2022Review
- Toward Human Models of Cardiorenal SyndromeFrontiers in cardiovascular medicine · 2022Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The extracellular matrix (ECM) plays important roles in maintaining physiological structure and functions of various tissues and organs. Cardiac fibrosis is the excess deposition of ECM, including both fibrillar (collagens I and III) and non-fibrillar proteins. Characteristics of fibrosis can vary depending on the pathology, with focal fibrosis occurring following myocardial infarction (MI), and diffuse interstitial and perivascular fibrosis mainly in non-ischemic heart diseases. Compliance of the fibrotic tissue is significantly lower than the normal myocardium, and this can compromise the diastolic, as well as systolic dysfunction. Therefore, strategies to combat cardiac fibrosis have been investigated. Upon injury or inflammation, activated cardiac fibroblasts (myofibroblasts) produce more ECM proteins and cause fibrosis. The activation could be inhibited or the myofibroblasts could be ablated by targeting their specific expressed proteins. Modulation of tissue inhibitors of metalloproteinases (TIMPs) and moderate exercise can also suppress cardiac fibrosis. More recently, sex differences in cardiac fibrosis have come to light with differential fibrotic response in heart diseases as well as in fibroblast functions
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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.