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Figure 7 | Fibrogenesis & Tissue Repair

Figure 7

From: Human lung myofibroblast TGFβ1-dependent Smad2/3 signalling is Ca2+-dependent and regulated by KCa3.1 K+ channels

Figure 7

The involvement of K Ca 3.1 in the TGF/Smad 2/3 signalling pathway. A diagrammatic representation of how Smad2/3 phosphorylation and subsequent nuclear translocation is reliant on an influx of extracellular Ca2+ and KCa3.1 ion channels. TGFβ1 stimulation triggers an influx of extracellular Ca2+, which in turns opens Ca2+-activated KCa3.1 K+ channels. KCa3.1 opening maintains a negative membrane which in turn promotes Ca2+ entry. Phosphorylation of Smad2/3 and therefore its downstream effects such as translocation and gene transcription are heavily reliant on Ca2+. KCa3.1 channel inhibition reduces Ca2+ entry, which in turn reduces Smad2/3 phosphorylation and nuclear translocation, and thus reduces TGFβ1-dependent gene transcription.

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