Piezo1 and tissue fibrosis: insights into its role and potential for modulation

Yuxin Lin , Dongsheng Wen , Kai Chen , Zhiang Hu , Chiakang Ho , Yangdan Liu , Zhiyuan Zhou , Ya Gao , Qingfeng Li , Yifan Zhang

Burns & Trauma ›› 2025, Vol. 13 ›› Issue (1) : tkaf054

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Burns & Trauma ›› 2025, Vol. 13 ›› Issue (1) :tkaf054 DOI: 10.1093/burnst/tkaf054
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Piezo1 and tissue fibrosis: insights into its role and potential for modulation
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Abstract

Fibrosis is a pathological process marked by excessive extracellular matrix deposition, ultimately resulting in irreversible tissue damage. This aberrant process manifests across multiple organs, including the skin, lung, cardiovascular system, liver, kidneys, and eyes. However, the underlying mechanisms driving tissue fibrosis remain incompletely elucidated, and effective therapeutics are still lacking. In recent years, increasing attention has turned toward the contribution of mechanical signals to fibrotic progression. Within this context, the Piezo family of mechanosensitive ion channels, recently identified as key mediators of mechanotransduction, has emerged as a compelling focus of investigation in diverse pathological settings. This review summarizes current evidence on the central role of Piezo1 in orchestrating fibrotic responses across various tissues. Moreover, we examine the application of Piezo1 modulators in experimental models and their potential to modulate fibrosis, thereby informing the development of novel antifibrotic interventions. By integrating mechanobiological insights into the study of fibrosis, this work highlights promising translational avenues for advancing therapeutic strategies and improving clinical outcomes in fibrotic disease.

Keywords

Piezo1 / Fibrosis / Biomechanics / Extracellular matrix

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Yuxin Lin, Dongsheng Wen, Kai Chen, Zhiang Hu, Chiakang Ho, Yangdan Liu, Zhiyuan Zhou, Ya Gao, Qingfeng Li, Yifan Zhang. Piezo1 and tissue fibrosis: insights into its role and potential for modulation. Burns & Trauma, 2025, 13 (1) : tkaf054 DOI:10.1093/burnst/tkaf054

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