Flow-dependent remodeling of blood vessels is critical for normal physiology and for recovery from arterial blockage in disease; understanding its cellular mechanisms may lead to the development of treatments for patients that are deficient in this process following myocardial infarction or other vascular diseases.

A threshold level of blood flow initiates developmental blood vessel regression; this threshold can be regulated by non-canonical Wnt ligands.

Local coordination between shear and hydrostatic stress regulates valve shape and size.

Cell protease and cell fate decisions are regulated by a bone fide force-sensor, the Piezo1 channel, and by this means achieve integration with the mechanical environment.

Relative hydraulic resistance, shear rate, and pressure in a vascular network integrate the network's architecture via fluid flow, and determine vein dynamics, with a time delay, in the prototypical organism Physarum polycephalum.

Nearly half of the transcriptome is altered when endothelial cells transition in vitro, expression patterns for some genes are regained by exposing cells to shear stress and others through exposure to smooth muscle cells.

Autonomous patterns of cell contraction in the context of localized apical extracellular matrix constraints specify tissue stresses that reshape the wing epithelium.

Under fluid shear, living cells deform elliptically, align in flow direction, and rotate, from which their frequency-dependent viscoelastic properties can be inferred.

Cell movement toward and away from the midline of an epithelium over tens of hours are caused by spontaneous or externally-applied shear forces to eliminate force imbalances within the tissue.

Net-winged midge larvae use suction organs covered in spine-like cuticular protrusions to generate powerful attachment on wet and rough surfaces.