ReviewJournal of clinical medicine2017
The Soft- and Hard-Heartedness of Cardiac Fibroblasts: Mechanotransduction Signaling Pathways in Fibrosis of the Heart.
Review in Journal of clinical medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 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
98 citing papers in PubMed, 171 citations in OpenAlex.
- Cardiac fibrosis: mechanistic insights and translational advances.Molecular biomedicine · 2026Review
- Arrhythmic Mitral Valve Prolapse as a Regional Stretch-Induced Cardiomyopathy with Fibro-Inflammatory Signature: A Conceptual Review.Journal of cardiovascular development and disease · 2026Review
- Biomechanical stress unmasks a fibroblast-dependent hypercontractile-disarray phenotype in MYBPC3 truncation HCM.APL bioengineering · 2026Article
- Rhythms of growth: unveiling the mechanobiology behind heart maturation.The Journal of physiology · 2026Review
- Cardiac mechanotransduction from development to disease.APL bioengineering · 2026Review
- Magnetic torque-mediated early asymmetric mechanical stimulation directs structural and functional maturation in human cardiac organoids.Scientific reports · 2026Article
- Review
- Changes in ovarian hardness and elasticity affect the development and function of secondary follicles.Scientific reports · 2026Article
- Mechanical Modeling of Cardiac Fibrosis With Explicit Spatial Representation of Cellular Structure and Collagen Alignment.Journal of biomechanical engineering · 2026Article
- Atrial fibroblast metabolic reprogramming in atrial fibrillation: a candidate mechanism within multicellular atrial cardiomyopathy.Frontiers in cardiovascular medicine · 2026Review
- ECM proteins regulate microRNA-mediated direct reprogramming of fibroblasts into cardiomyocytes via YAP signaling.Frontiers in bioengineering and biotechnology · 2026Article
- Article
- Mechanical Stress Triggers Premature Senescence in Cardiac Fibroblasts.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- From fibro/adipogenic progenitors to adipocytes: Understanding adipogenesis in muscle degeneration for disease modulation.The Journal of physiology · 2025Review
- Piezo1 in heart failure: A new perspective from cytomechanical sensing to diverse cellular pathways.Molecular biology reports · 2025Review
- Decoding mechanosensitive genes in cardiac fibroblasts via 3D hydrogel models of fibrosis.Scientific reports · 2025Article
- Increased matrix stiffness promotes fibrogenesis of hepatic stellate cells through AP-1-induced chromatin priming.Communications biology · 2025Article
- Dressed in Collagen: 2D and 3D Cardiac Fibrosis Models.International journal of molecular sciences · 2025Review
- Piezo1 and tissue fibrosis: insights into its role and potential for modulation.Burns & trauma · 2025Review
- 3D matrix stiffness modulation unveils cardiac fibroblast phenotypic switching.Scientific reports · 2024Article
38 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Cardiac fibrosis, the excessive accumulation of extracellular matrix (ECM), remains an unresolved problem in most forms of heart disease. In order to be successful in preventing, attenuating or reversing cardiac fibrosis, it is essential to understand the processes leading to ECM production and accumulation. Cardiac fibroblasts are the main producers of cardiac ECM, and harbor great phenotypic plasticity. They are activated by the disease-associated changes in mechanical properties of the heart, including stretch and increased tissue stiffness. Despite much remaining unknown, an interesting body of evidence exists on how mechanical forces are translated into transcriptional responses important for determination of fibroblast phenotype and production of ECM constituents. Such mechanotransduction can occur at multiple cellular locations including the plasma membrane, cytoskeleton and nucleus. Moreover, the ECM functions as a reservoir of pro-fibrotic signaling molecules that can be released upon mechanical stress. We here review the current status of knowledge of mechanotransduction signaling pathways in cardiac fibroblasts that culminate in pro-fibrotic gene expression.
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.