Piezo mechanosensitive channels: A biological hub for intestinal barrier homeostasis and an emerging target for disease intervention

Table 2 Pathogenic mechanisms of piezo channel in inflammatory bowel disease

Pathogenic mechanism	Related pathways	Specific effect
Inflammatory regulation	Elevated expression of Piezo1 induces Ca2+ influx in HT29 cells, leading to ROS accumulation and activation of NLRP3 inflammasome[14]	Intestinal inflammation worsens; impaired intestinal barrier function; worsening of oxidative stress injury in intestinal epithelium
	Piezo1 regulates aerobic glycolysis in macrophages and enhances LPS-induced immune responses. Additionally, Piezo1 can increase the levels of IL-6, TNF-α, and IL-1β[43]	The pro-inflammatory immune response of macrophages is exacerbated; increased secretion of inflammatory cytokines
	In IECs, Piezo1 activation induces Ca2+ influx and leads to ATP secretion, promoting the secretion of immune factors such as IL-8, and regulates modulatory genes in immune pathways[52]	Disruption of immune pathway regulation exacerbates inflammatory responses
Immunodeficiency	The absence of Piezo1 promotes the polarization of Th1 and Th17 cells, leading to reduced inflammatory signaling[70]	Pathogenic T-cell inflammatory response is attenuated, alleviating inflammation

ROS: Reactive oxygen species; LPS: Lipopolysaccharide; IL-6: Interleukin-6; TNF-α: Tumor necrosis factor alpha; IL-1β: Interleukin-1β; IECs: Intestinal epithelial cells; IL-8: Interleukin-8; Th1: Type 1 helper T cell; Th17: T helper 17 cells.