ArticlePhysiological reports2018
Hydrostatic pressure suppresses fibrotic changes via Akt/GSK-3 signaling in human cardiac fibroblasts.
Article in Physiological reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- Differential Transcriptomic and Adhesion Responses of Human Periodontal Ligament Cells to Cyclic and Static Hydrostatic Pressure.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Modelling and targeting mechanical forces in organ fibrosis.Nature reviews bioengineering · 2024Article
- Cellular signaling pathways in the nervous system activated by various mechanical and electromagnetic stimuli.Frontiers in molecular neuroscience · 2024Review
- Role of non-cardiomyocytes in anticancer drug-induced cardiotoxicity: A systematic review.iScience · 2022Review
- Hydrostatic pressure induces profibrotic properties in hepatic stellate cells via the RhoA/ROCK signaling pathway.FEBS open bio · 2022Article
- Store-operated calcium entry via ORAI1 regulates doxorubicin-induced apoptosis and prevents cardiotoxicity in cardiac fibroblasts.PloS one · 2022Article
- Crosstalk between GSK-3β-actuated molecular cascades and myocardial physiology.Heart failure reviews · 2021Review
- Crosstalk of Diabetic Conditions with Static Versus Dynamic Flow Environment-Impact on Aortic Valve Remodeling.International journal of molecular sciences · 2021Article
- Reactive fibrosis precedes doxorubicin-induced heart failure through sterile inflammation.ESC heart failure · 2020Article
- Prostaglandin ECancer science · 2020Article
- Doxorubicin induces trans-differentiation and MMP1 expression in cardiac fibroblasts via cell death-independent pathways.PloS one · 2019Article
- Alternating magnetic field enhances cytotoxicity of Compound C.Cancer science · 2018Article
- Hydrostatic pressure suppresses fibrotic changes via Akt/GSK-3 signaling in human cardiac fibroblasts.Physiological reports · 2018Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mechanical stresses play important roles in the process of constructing and modifying heart structure. It has been well established that stretch force acting on cardiac fibroblasts induces fibrosis. However, the effects of compressive force, that is, hydrostatic pressure (HP), have not been well elucidated. We thus evaluated the effects of HP using a pressure-loading apparatus in human cardiac fibroblasts (HCFs) in vitro. In this study, high HP (200 mmHg) resulted in significant phosphorylation of Akt in HCFs. HP then greatly inhibited glycogen synthase kinase 3 (GSK-3)α, which acts downstream of the PI3K/Akt pathway. Similarly, HP suppressed mRNA transcription of inflammatory cytokine-6, collagen I and III, and matrix metalloproteinase 1, compared with an atmospheric pressure condition. Furthermore, HP inhibited collagen matrix production in a three-dimensional HCF culture. Taken together, high HP suppressed the differentiation of fibroblasts into the myofibroblast phenotype. HP under certain conditions suppressed cardiac fibrosis via Akt/GSK-3 signaling in HCFs. These results might help to elucidate the pathology of some types of heart disease.
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