Key result
Acute hyperthermia at 42 °C directly inhibits TGF-β1-mediated activation of human cardiac fibroblasts and prevents cardiac fibrosis in an Ang II infusion mouse model via suppression of Akt/S6K signaling.
Why the study?
Does hyperthermia inhibit TGF-β1-induced cardiac fibroblast activation and cardiac fibrosis?
Does hyperthermia inhibit TGF-β1-induced cardiac fibroblast activation and cardiac fibrosis?
Acute hyperthermia directly inhibits TGF-β-mediated activation of human cardiac fibroblasts and prevents cardiac fibrosis in vivo by suppressing Akt/S6K signaling.
Answers are grounded in this paper and cite their sources.
Hyperthermia may inhibit cardiac fibroblast activation; leaves open translation to human fibrosis prevention.
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.
No takes yet. Share an insight, caveat, or question.
Narikawa et al. (2018) studied Cardiac fibrosis. Hyperthermia (42 °C) vs. Normal saline or 37 °C / 39 °C was evaluated on IL-6 production, α-SMA expression, and collagen synthesis. Acute hyperthermia at 42 °C directly inhibits TGF-β1-mediated activation of human cardiac fibroblasts and prevents cardiac fibrosis in an Ang II infusion mouse model via suppression of Akt/S6K signaling.
Synapse has enriched 10 related papers. Consider them for comparative context: