ArticleScientific reports2018
Acute Hyperthermia Inhibits TGF-β1-induced Cardiac Fibroblast Activation via Suppression of Akt Signaling.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 27 citations in OpenAlex.
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- Orai1- and STIM1-mediated calcium signaling controls PD-L1 expression and modulates antitumor immunity in oral cancer.The journal of physiological sciences : JPS · 2026Article
- 7-nm MnTheranostics · 2025Article
- Alternative magnetic field exposure suppresses tumor growth via metabolic reprogramming.Cancer science · 2024Article
- Detection and management of latent rheumatic heart disease: a narrative review.Annals of medicine and surgery (2012) · 2023Review
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- Store-operated calcium entry via ORAI1 regulates doxorubicin-induced apoptosis and prevents cardiotoxicity in cardiac fibroblasts.PloS one · 2022Article
- CDK6 is stimulated by hyperthermia and protects gastric cancer cells from hyperthermia‑induced damage.Molecular medicine reports · 2021Article
- Signalling pathways implicated in the pathogenesis of rheumatic heart disease (Review).Experimental and therapeutic medicine · 2021Review
- Reactive fibrosis precedes doxorubicin-induced heart failure through sterile inflammation.ESC heart failure · 2020Article
- Prostaglandin ECancer science · 2020Article
- Anti-interleukin-6 receptor antibody treatment ameliorates postoperative adhesion formation.Scientific reports · 2019Article
- 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 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transforming growth factor-β1 (TGF-β1) induces phenotypic changes in fibroblasts to become myofibroblasts with increased production of extracellular matrix (ECM) components and cytokines. It is also known that excessive activation of myofibroblasts accelerates cardiac fibrosis, remodeling, and thus cardiac dysfunction. However, no effective therapy has been established to prevent this process although recent clinical studies have demonstrated the effectiveness of hyperthermia in cardiac dysfunction. The aim of this study was to examine the molecular mechanism of hyperthermia on TGF-β1-mediated phenotypic changes in cardiac fibroblasts. TGF-β1 increased the expression of IL-6, α-smooth muscle actin (α-SMA), and collagen in human cardiac fibroblasts (HCFs). Hyperthermia (42 °C) significantly prevented these changes, i.e., increases in IL-6, α-SMA, and collagen, as induced by TGF-β1 in a time-dependent manner. Immunoblotting showed that hyperthermia decreased Akt/S6K signaling, but did not affect Smad2 and Smad3 signaling. Pharmacological inhibition of Akt signaling mimicked these effects of hyperthermia. Furthermore, hyperthermia treatment prevented cardiac fibrosis in Ang II infusion mice model. Putting together, our findings suggest that hyperthermia directly inhibits TGF-β-mediated activation of HCFs via suppressing Akt/S6K signaling.
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