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Related Experiment Video

Updated: May 15, 2026

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

Adiponectin promotes functional recovery after podocyte ablation.

Joseph M Rutkowski¹, Zhao V Wang, Ae Seo Deok Park

¹Touchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.

Journal of the American Society of Nephrology : JASN

|January 22, 2013

Summary

Adiponectin, a protein from fat cells, protects kidneys from injury. Studies show it aids recovery after podocyte damage, preventing irreversible kidney failure.

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Generation of Patient-Derived Podocytes from Skin Biopsies

Generation of Patient-Derived Podocytes from Skin Biopsies

Published on: May 26, 2023

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Last Updated: May 15, 2026

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

Generation of Patient-Derived Podocytes from Skin Biopsies

Generation of Patient-Derived Podocytes from Skin Biopsies

Published on: May 26, 2023

Area of Science:

Nephrology
Endocrinology
Molecular Biology

Background:

Low adiponectin levels correlate with albuminuria in humans and mice.
The specific role of adiponectin in the progression of kidney disease remains unclear.

Purpose of the Study:

To investigate the causative role of adiponectin in modulating podocyte injury and renal disease.
To establish a novel mouse model for studying podocyte-specific injury and regeneration.

Main Methods:

Generation of POD-ATTAC mice for inducible, podocyte-specific apoptosis via caspase-8.
Crossing POD-ATTAC mice with adiponectin-deficient or overexpressing mouse lines.
Assessment of kidney damage, albuminuria, renal function, and interstitial fibrosis.

Main Results:

POD-ATTAC mice developed significant kidney damage, including foot process effacement and glomerulosclerosis.
Mice lacking adiponectin showed irreversible albuminuria and renal failure post-injury.
Mice overexpressing adiponectin exhibited faster recovery and reduced fibrosis after podocyte injury.

Conclusions:

Adiponectin acts as a renoprotective factor following podocyte injury.
The POD-ATTAC mouse model enables precise temporal control of podocyte injury and regeneration studies.