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Related Experiment Video

Updated: Jan 10, 2026

Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells

Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells

Published on: November 21, 2025

Androgens Drive SOX9 Upregulation in Injured Proximal Tubular Cells.

Corynne Vermillion Allison¹, Prisha S Patel², Qiao Xuanyuan³

¹Division of Pharmaceutics and Pharmacology, College of Pharmacy & Comprehensive Cancer Center, Ohio State University, Columbus, OH, USA.

Biorxiv : the Preprint Server for Biology

|November 24, 2025

Summary

Male kidneys utilize a testosterone-driven SOX9 repair pathway after acute kidney injury (AKI), which is absent in females. This highlights sex-specific differences in kidney repair mechanisms and the need for tailored AKI treatments.

Keywords:

Sox9 (sex-determining region Y [SRY] box 9)acute kidney injury (AKI)cisplatin ischemia proximal tubules (PTs)

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Area of Science:

Nephrology
Molecular Biology
Endocrinology

Background:

Sex significantly impacts acute kidney injury (AKI) susceptibility and outcomes.
Most rodent AKI models focus on males, limiting understanding of female-specific responses.
The transcription factor SOX9 plays a role in male AKI repair but its sex-specific function is unexplored.

Purpose of the Study:

Investigate if SOX9 mediates sex-specific tubular responses in adult kidneys following AKI.
Determine the role of SOX9 and related factors in sex-dependent kidney injury and repair.
Elucidate the regulatory networks involved in sex-specific AKI responses.

Main Methods:

Optimized ischemic and cisplatin AKI models in male and female rodents.
Utilized tubule-specific knockout models for Sox9, Sox4, Sox11, Vgf, Zfp24, and androgen receptor (Ar).
Conducted gonadectomy and hormone replacement studies, alongside gene and protein analyses.

Main Results:

SOX9 and Vgf induction were significantly blunted in female kidneys post-AKI compared to males.
Zfp24 was functionally relevant only in males, while Sox4 and Sox11 were protective in both sexes.
Testosterone signaling, via AR, was essential for SOX9 induction in males, establishing a male-specific repair axis.

Conclusions:

A male-specific, testosterone-dependent tubular repair program exists in AKI.
Kidney injury and recovery pathways differ fundamentally between sexes.
Sex-inclusive therapeutic strategies are crucial for effective AKI treatment.