Mechanosensitive channels Piezo1/2 are required for osteoblast differentiation from progenitors by sensing fluid sheer stress and matrix rigidity and regulating NFATc1, YAP1 and ß-catenin activities through Ca²⁺ stimulated phosphatase calcineurin.

A functionally conserved inactivation gate in the inner helix of Piezo channels controls the majority of the inactivation process via a hydrophobic mechanism.

Depletion of the mechanosensitive ion channel PEZO-1 in C. elegans disrupts the sheath and spermathecae cells to disrupt oocyte ovulation, resulting in crushed oocytes.

A chemical activator of the mechanosensitive Piezo1 ion channel has been identified.

Tension is the activating stimulus of Piezo1 mechanosensitive ion channels and resting membrane tension modulates overall channel sensitivity to mechanical stimulation.

Local Mtmr2 activity and PI(3,5)P2 abundance dynamically control Piezo2-dependent mechanotransduction in peripheral sensory neurons.

Super-resolution microscopy and single particle tracking analysis of Piezo1 in red blood cells demonstrate its ability to sense membrane curvature, consistent with a force-through-membrane mechanism of channel mechanosensation in these cells.

Piezo1 ion channels are not modulated by RNA ligands, contrary to previous findings.

Mechanical stimuli activate Piezo1 in osteoblast lineage cells and thereby promote bone formation in part via Wnt1.

Piezo1 exhibits markedly different kinetic behavior in different cellular contexts.