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Science Paper Examines Molecular Contributors to Kidney Fibrosis

A genetic study of mice and humans in this week's Science Signaling has identified new molecular contributors to kidney fibrosis. Chronic kidney disease and kidney injury often result in renal fibrosis, but the mechanisms underlying fibrogenesis are not entirely clear. In the study, a University of Manchester-led team used RNA sequencing and other techniques to study kidney fibrosis in human patients and in mice with experimentally induced kidney injury. They found that the transcription factor SOX9 is involved in fibrosis in both the humans and the animals, with Neuron navigator 3 (NAV3) acting downstream of SOX9. In mice, knocking out Sox9 reduced injury-induced kidney fibrosis and an associated increase in Nav3 expression, while experiments in an in vitro model of renal pericyte transdifferentiation into myofibroblasts showed that NAV3 is required for multiple aspects of fibrogenesis. "Our work identifies a SOX9-NAV3-YAP1 axis involved in the progression of kidney fibrosis and points to NAV3 as a potential target for pharmacological intervention," the study's authors write.

The Scan

Genetic Testing Approach Explores Origins of Blastocyst Aneuploidy

Investigators in AJHG distinguish between aneuploidy events related to meiotic missegregation in haploid cells and those involving post-zygotic mitotic errors and mosaicism.

Study Looks at Parent Uncertainties After Children's Severe Combined Immunodeficiency Diagnoses

A qualitative study in EJHG looks at personal, practical, scientific, and existential uncertainties in parents as their children go through SCID diagnoses, treatment, and post-treatment stages.

Antimicrobial Resistance Study Highlights Key Protein Domains

By screening diverse versions of an outer membrane porin protein in Vibrio cholerae, researchers in PLOS Genetics flagged protein domain regions influencing antimicrobial resistance.

Latent HIV Found in White Blood Cells of Individuals on Long-Term Treatments

Researchers in Nature Microbiology find HIV genetic material in monocyte white blood cells and in macrophages that differentiated from them in individuals on HIV-suppressive treatment.