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Testicular microcalcifications arise secondary to local alterations in mineral homeostasis, which in combination with impaired Sertoli cell function and reduced levels of mineralization inhibitors facilitate deposition of hydroxyapatite.

Disruption of RAS–p110α signalling in macrophages impairs both the initiation and resolution of inflammatory responses, revealing a critical regulatory role in immune function and inflammation control.

Islet cholesterol levels determine GLP-1R function, with several cholesterol-binding sites mapped in active vs inactive receptors and one, containing Val229, shown to control GLP-1R behaviour in beta cell models.

Pyruvate and related metabolites are linked to reduced glaucoma risk among genetically predisposed individuals and mitigate disease in a mouse model, highlighting a potential metabolic mechanism of resilience.

Cell crowding drives a pro-invasive mechanotransduction pathway in high-grade DCIS, inducing TRPV4 inhibition, calcium and cell volume reduction, and increased invasion, with compensatory plasma-membrane TRPV4 relocation indicating pathway activation.

Cell crowding causes high-grade breast cancer cells to become more invasive by activating a molecular switch that causes the cells to shrink and spread.

Diet-induced obesity, insulin resistance, and proinflammatory macrophage activation and accumulation in adipose tissue can be counteracted through the inhibition of ER stress sensor IRE1alpha.

TRPγ is essential for maintaining lipid homeostasis in Drosophila melanogaster, linking neuronal regulation to fat metabolism and suggesting potential therapeutic avenues for metabolic disorders.