Large-scale in vivo imaging of the zebrafish left-right organizer (Kupffer's vesicle) combined with fluid dynamics calculations allows to quantitatively test the possible flow detection mechanisms and supports the flow transport of chemical signals as the mechanism of side determination.

Planarians provide evidence for a common evolutionary origin of vertebrate and invertebrate excretory systems and provide a novel experimental model to study human kidney diseases.

PKD2 (polycystin-2) channels are a major component of a flow-sensing signaling mechanism in endothelial cells that stimulates vasodilation and reduces blood pressure.

A hydrodynamic model of fish swimming in a channel predicts a critical flow speed for fish to successfully swim against a flow, unveiling a passive mechanism for rheotaxis to emerge without access to any sensory information.

Genetic studies reveal that mosaic inactivation of ccm2 causes characteristic cerebral cavernous malformations in adult zebrafish and aberrant responses to blood flow that induce the formation of a lethal embryonic multi-cavernous venous malformation.

Retention of genetic diversity at immune-related loci drives the pattern of genetic variation in selfing Capsella.

Flow stimulates PC-1/PC-2 clusters in the plasma membrane of endothelial cells, leading to Ca²⁺ influx, NOS, SK channel, and IK channel activation, vasodilation, and a reduction in blood pressure.

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

SWELL1 is required for basal, stretch, and flow-mediated endothelial AKT-eNOS signaling in vitro and protects against angiotensin-induced hypertension and diabetes-associated vascular dysfunction in vivo.

An interaction between the ion channel ASIC1a and the protein RIP1 is responsible for neuronal death caused by tissue acidosis.