Table 1 In vitro and in vivo studies the roles of mechanosensitive ion channels (MSCs) in ALI/ARDS

ENaC

Alveolar epithelial cells

Promotes alveolar fluid clearance and attenuates pulmonary edema

[75, 77, 78]

Endothelial cells

Protects endothelial barrier function

[83, 84]

Piezo1

Alveolar epithelial cells

Triggers alveolar type I cells ATP release and paracrine stimulation of surfactant secretion from alveolar type II cells

[53]

Induces alveolar type II cells apoptosis

[54]

Endothelial cells

Activation of Piezo1 disrupts endothelial adherens junction proteins and causes endothelial hyperpermeability

[29, 49]

Protects adherens junction and matains endothelial barrier function

[50]

Endothelial Piezo1-mediated Ca²⁺ influx stimulates neutrophil extravasation

[100]

Macrophages

Enhances macrophage phagocytosis and promotes bacterial clearance

[45]

TRPV4

Alveolar epithelial cells

Activation of TRPV4 disrupts epithelial barrier function

[37, 112]

Maintains epithelial barrier function

[31]

Endothelial cells

Activation of TRPV4 disrupts endothelial barrier function

[111, 112]

Macrophages

Lipopolysaccharide/matrix stiffness-induced macrophage phagocytosis in vitro and in vivo

[7, 42]

Anti-inflammatory cytokine production (IL-1β, IL-10)

TRPV1/TRPA1

Immune cells (macrophages, neutrophils)

Elevates ROS production,activates MAPK/NF-κB signaling, increases proinflammatory mediators and aggravates inflammatory response

[115]

TRPC1

Endothelial cells

Disrupts adherens junction and induces endothelial hyperpermeability

[116]

TRPC6

Endothelial cells

Induces endothelial hyperpeamability

[109, 117]

TRPM2

Macrophages

Decreases the ROS production and reduces pro-inflammatory cytokine and chemokine release

[118]

TREK-1

Alveolar epithelial cells

Decreases cell deformability and inhibit stretch-induced cell detachment

[126]

Stimulates cell proliferation

[127]

Anti-inflammatory cytokine production (↓IL-6 and ↑MCP-1)

[127, 128]

Hyperoxia exposure decreases the TREK-1 expression

[36]