ReviewAgeing research reviews2020
Mechanosensing dysregulation in the fibroblast: A hallmark of the aging heart.
Review in Ageing research reviews, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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
41 citing papers in PubMed, 70 citations in OpenAlex.
- From aging biology to cardiac biotechnology: emerging platforms for modeling cardiac aging.JCI insight · 2026Review
- Aging of hair follicle stem cells and their niche: mechanisms and regenerative therapeutic strategies.Cell communication and signaling : CCS · 2026Review
- Versican regulating viscoelasticity drives pleural fibrosis via mechanotransductive signaling.JCI insight · 2026Article
- Musculoskeletal degeneration and cardiovascular aging: a narrative review of shared mechanobiological pathways.Molecular biology reports · 2026Review
- Patches: A Representation Learning Framework for Decoding Shared and Condition-Specific Transcriptional Programs in Wound Healing.bioRxiv : the preprint server for biology · 2026Article
- HNF4A P2 isoform alleviates kidney fibrosis by inhibiting dedifferentiation of proximal tubular cells through JAG1/NOTCH signaling.Cellular & molecular biology letters · 2026Article
- Self-organizing three-dimensional dermal papilla cell spheroids yield therapeutic extracellular vesicles that target hypertrophic scar regression via the miR-26a-5p/CCNE2 axis.Burns & trauma · 2026Article
- Hydrogen Sulfide Ameliorates Heart Aging by Downregulating Matrix Metalloproteinase-9.Cardiovascular drugs and therapy · 2025Article
- PFKFB3 Promotes Myofibroblast Differentiation and Cardiac Fibrosis Through its Intra- and Extra- Cellular Roles.Journal of cardiovascular translational research · 2025Article
- Hybrid hydrogel-extracellular matrix scaffolds identify biochemical and mechanical signatures of cardiac ageing.Nature materials · 2025Article
- Matrix stiffness regulates nucleus pulposus cell glycolysis by MRTF-A-dependent mechanotransduction.Bone research · 2025Article
- Article
- FBLN7 KO attenuates age-related cardiac fibrosis by promoting TGFBR3/ALK1/Smad1 signaling and inhibiting the profibrotic phenotypes of cardiac fibroblasts.Theranostics · 2025Article
- Decellularized Green and Brown Macroalgae as Cellulose Matrices for Tissue Engineering.Journal of functional biomaterials · 2024Article
- Disability level's impact on blood pressure-mortality association in older long-term care adults: evidence from a large Chinese cohort study.BMC geriatrics · 2024Article
- Cardiac and perivascular myofibroblasts, matrifibrocytes, and immune fibrocytes in hypertension; commonalities and differences with other cardiovascular diseases.Cardiovascular research · 2024Review
- Roles of Integrin in Cardiovascular Diseases: From Basic Research to Clinical Implications.International journal of molecular sciences · 2024Review
- The Senescent Heart-"Age Doth Wither Its Infinite Variety".International journal of molecular sciences · 2024Review
- [Influences and mechanism of extracellular vesicles from dermal papilla cells of mice on human hypertrophic scar fibroblasts].Zhonghua shao shang yu chuang mian xiu fu za zhi · 2024Article
- AMPK signaling inhibits the differentiation of myofibroblasts: impact on age-related tissue fibrosis and degeneration.Biogerontology · 2024Review
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 2 institutions in 2 countries.
Funding
Abstract
The myofibroblast is a specialized fibroblast that expresses α-smooth muscle actin (α-SMA) and participates in wound contraction and fibrosis. The fibroblast to myofibroblast transition depends on chemical and mechanical signals. A fibroblast senses the changes in the environment (extracellular matrix (ECM)) and transduces these changes to the cytoskeleton and the nucleus, resulting in activation or inhibition of α-SMA transcription in a process called mechanosensing. A stiff matrix greatly facilitates the transition from fibroblast to myofibroblast, and although the aging heart is much stiffer than the young one, the aging fibroblast has difficulties in transitioning into the contractile phenotype. This suggests that the events occurring downstream of the matrix, such as activation or changes in expression levels of various proteins participating in mechanotransduction can negatively alter the ability of the aging fibroblast to become a myofibroblast. In this review, we will discuss in detail the changes in ECM, receptors (integrin or non-integrin), focal adhesions, cytoskeleton, and transcription factors involved in mechanosensing that occur with aging.
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.