Negative pressure-induced fibroblast activation for wound healing through the Piezo1-Ca²⁺-NFAT3 signaling pathway

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Background Negative pressure wound therapy (NPWT) is widely used to promote wound healing, yet the mechanotransduction mechanisms underlying its efficacy remain unclear because of the absence of precise and controllable in vitro negative pressure loading devices for cellular-level studies. Therefore, this study aims to develop a precise and controllable in vitro negative pressure loading device and to elucidate the mechanotransduction mechanism by which negative pressure activates dermal fibroblasts during wound healing. Methods We developed a high-precision negative pressure loading device compatible with six-well plates, facilitating independent and intelligent control over negative pressure values, durations, and modes for each well. To validate the uniformity and stability of the negative pressure environment, finite element analysis (FEA) was implemented. The mechanism was explored using proteomic profiling of negative pressure-treated fibroblasts, complemented by molecular interrogation of Piezo1 expression and calcium signaling dynamics. The results of functional studies integrated genetic silencing and pharmacological modulation of the pathway, with in vivo confirmation through SD rat-based NPWT experiments. Results FEA confirmed a stable pressure distribution within the negative pressure chamber. The cells experienced predominantly compressive stresses that scaled line

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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