- Design
- Experimental study in mice with tubule-specific knockouts
- Population
- Male and female mice with matched ischaemic or cisplatin AKI
- Primary outcome
- Sex-specific tubular repair responses
- Effect
- SOX9 induced only in males via androgen receptor; deletion worsened injury in males only
A Kidney International experimental study compared male and female mice given matched ischaemic or cisplatin kidney injury.
Standard injury markers, NGAL and KIM-1, rose equally in both sexes. But the repair factor SOX9 and its target VGF were induced strongly only in males. Deleting SOX9 or its regulators worsened injury in males but not females. Castration or deleting the androgen receptor in tubules abolished SOX9 induction. Two related factors, SOX4 and SOX11, were protective in both sexes.
Human AKI outcomes differ by sex, and most experimental work has used male animals. This study suggests the repair biology itself differs, so a drug targeting SOX9 could work in one sex and not the other.
This is preclinical work with no direct clinical application yet. Its importance is for trial design: AKI therapies should be tested in both sexes.
- Treat this as mechanistic research, not a basis for changing AKI care
- Expect future AKI drug trials to report results by sex
- Note that standard biomarkers such as NGAL and KIM-1 behaved the same in both sexes
Why it matters
A treatment developed in male models may not work the same way in women.
Don't overread it
Mouse data: it does not show that men and women recover differently for this reason.
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