Volume 5 Issue 12, December 2021

Softening the surface of silicone implants reduces their fibrotic encapsulation.

In tendon cells under shear stress, the induction of an influx of calcium by the mechanosensitive ion channel PIEZO1 upregulates collagen crosslinking, which increases tendon stiffness and potentially improves jumping performance.

Cancer cells enriched in cholesterol in their plasma membrane impair T-cell-mediated cytotoxicity, which can be augmented by stiffening the cancer cells via cholesterol depletion, as shown in mouse models of adoptive T-cell immunotherapy.

In metastatic lymph nodes, solid stress generated by metastatic growth prevents the infiltration of lymphocytes into the lesions.

The fibrotic encapsulation of subcutaneous silicone implants in mice can be suppressed by softening the implant surface or inhibiting the integrin-mediated activation of transforming growth factor beta 1.

The mechanosensitive ion channel PIEZO1 senses shear stress induced by collagen-fibre sliding in tendons, regulates their stiffness and influences jumping performance.

A dysfunctional TRPV4–GSK3β pathway in osteoarthritic chondrocytes renders the cells unable to respond to viscoelastic changes in the extracellular matrix.

Cumulative tension on the nuclear membrane of aortic fibroblasts resulting from increases in the stiffness of the extracellular matrix transforms transiently activated fibroblasts into fibrosis-driving myofibroblasts with condensed chromatin.

Strain maps of cardiomyocyte nuclei during contraction indicate that, by integrating environmental mechanical cues, the nuclei of cardiomyocytes stabilize the fate of cells through the reorganization of epigenetically marked chromatin.