ReviewJournal of cell science2015
Mechanobiology of myofibroblast adhesion in fibrotic cardiac disease.
Review in Journal of cell science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 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
76 citing papers in PubMed, 129 citations in OpenAlex.
- Branched-chain amino acid transaminase 1-mediated pathway promotes proline-dependent collagen production in cardiac myofibroblasts.The Journal of clinical investigation · 2026Article
- Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026Review
- A Comprehensive Review: Unraveling the Role of Inflammation in the Etiology of Heart Failure.Heart failure reviews · 2025Review
- Blockade of YAP Mechanoactivation Prevents Neointima Formation and Adverse Remodeling in Arterialized Vein Grafts.Journal of the American Heart Association · 2025Article
- Association of theInternational journal of molecular sciences · 2025Article
- The mechanotransduction-immune axis in organ fibrosis: dual regulatory mechanisms and translational therapeutic perspectives.Frontiers in immunology · 2025Review
- Fibrotic extracellular matrix impacts cardiomyocyte phenotype and function in an iPSC-derived isogenic model of cardiac fibrosis.Translational research : the journal of laboratory and clinical medicine · 2024Article
- The motor-clutch model in mechanobiology and mechanomedicine.Mechanobiology in medicine · 2024Review
- 3D matrix stiffness modulation unveils cardiac fibroblast phenotypic switching.Scientific reports · 2024Article
- The local mechanosensitive response of primary cardiac fibroblasts is influenced by the microenvironment mechanics.Scientific reports · 2024Article
- Roles of Integrin in Cardiovascular Diseases: From Basic Research to Clinical Implications.International journal of molecular sciences · 2024Review
- Cardiovascular human organ-on-a-chip platform for disease modeling, drug development, and personalized therapy.Journal of biomedical materials research. Part A · 2024Review
- Article
- 3D bioprinted aged human post-infarct myocardium tissue model.Health science reports · 2024Article
- Mechanoregulation and function of calponin and transgelin.Biophysics reviews · 2024Review
- An Inverse Modeling Approach to Estimate Three-Dimensional Aortic Valve Interstitial Cell Stress Fiber Force Levels.Journal of biomechanical engineering · 2023Article
- Construction of cardiac fibrosis for biomedical research.Smart medicine · 2023Review
- Cardiac fibroblasts and mechanosensation in heart development, health and disease.Nature reviews. Cardiology · 2023Review
- Nicotinamide riboside kinase-2 regulates metabolic adaptation in the ischemic heart.Journal of molecular medicine (Berlin, Germany) · 2023Article
- Stomatin-like protein 2 deficiency exacerbates adverse cardiac remodeling.Cell death discovery · 2023Article
16 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Fibrotic cardiac disease, a leading cause of death worldwide, manifests as substantial loss of function following maladaptive tissue remodeling. Fibrosis can affect both the heart valves and the myocardium and is characterized by the activation of fibroblasts and accumulation of extracellular matrix. Valvular interstitial cells and cardiac fibroblasts, the cell types responsible for maintenance of cardiac extracellular matrix, are sensitive to changing mechanical environments, and their ability to sense and respond to mechanical forces determines both normal development and the progression of disease. Recent studies have uncovered specific adhesion proteins and mechano-sensitive signaling pathways that contribute to the progression of fibrosis. Integrins form adhesions with the extracellular matrix, and respond to changes in substrate stiffness and extracellular matrix composition. Cadherins mechanically link neighboring cells and are likely to contribute to fibrotic disease propagation. Finally, transition to the active myofibroblast phenotype leads to maladaptive tissue remodeling and enhanced mechanotransductive signaling, forming a positive feedback loop that contributes to heart failure. This Commentary summarizes recent findings on the role of mechanotransduction through integrins and cadherins to perpetuate mechanically induced differentiation and fibrosis in the context of cardiac disease.
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.