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Related Experiment Video

Updated: May 12, 2026

Assessment of Kidney Function in Mouse Models of Glomerular Disease

Assessment of Kidney Function in Mouse Models of Glomerular Disease

Published on: June 30, 2018

Diabetic nephropathy: lessons from the mouse.

Himanshu Vashistha¹, Leonard Meggs

¹Nephrology Research Laboratory, Institute of Translational Research, and.

Ochsner Journal

|March 28, 2013

Summary

This summary is machine-generated.

Deleting the p66 longevity gene in Akita mice protects kidneys from diabetic injury by reducing oxidative stress and improving podocyte survival. This novel model offers insights into diabetic nephropathy pathogenesis and potential therapeutic targets.

Keywords:

Diabetic nephropathies oxidative stress p66Shc protein proteinuria

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Area of Science:

* Molecular biology
* Genetics
* Nephrology

Background:

* Diabetic nephropathy lacks accurate mouse models for target identification.
* Oxidative stress and cellular damage are key in diabetic kidney disease progression.

Purpose of the Study:

* To develop a novel mouse model for diabetic nephropathy.
* To investigate the role of the p66 longevity gene in diabetic kidney disease.

Main Methods:

* Developed novel Akita diabetic mice with p66 gene deletion via homologous recombination.
* Analyzed kidney protection phenotypes, oxidative stress markers, and albuminuria.
* Investigated the interplay between Sirtuin 1 (SIRT1) and p53/FOXO3a pathways.

Main Results:

* p66 null Akita mice showed reduced oxidative stress, glomerular/tubular injury, and albuminuria.
* Podocyte survival was enhanced, preventing foot process effacement.
* SIRT1 upregulation in p66 null mice decreased p53 acetylation and promoted ROS-detoxifying gene transcription.

Conclusions:

* p66 deletion confers significant kidney protection in a diabetic mouse model.
* Findings highlight the p66/SIRT1/p53/FOXO3a axis in diabetic nephropathy.
* Future research will translate these findings to clinical diabetic nephropathy treatment.