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Related Experiment Video

Updated: Sep 1, 2025

Author Spotlight: Generation of Patient-Derived Podocytes from Skin Biopsies

Author Spotlight: Generation of Patient-Derived Podocytes from Skin Biopsies

Published on: May 26, 2023

Aged glomeruli: a link between PD-1 and podocytes.

Samuel Mon-Wei Yu¹, John Cijiang He^1,2,3

¹Division of Nephrology, Department of Medicine, and.

The Journal of Clinical Investigation

|August 15, 2022

Summary

This summary is machine-generated.

Kidney aging leads to podocyte damage. Blocking programmed death-1 (PD-1) signaling reverses aging in mouse kidneys and reduces proteinuria, suggesting new therapies for kidney disease.

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Guided Differentiation of Mature Kidney Podocytes from Human Induced Pluripotent Stem Cells Under Chemically Defined Conditions

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Published on: July 2, 2020

Area of Science:

Nephrology
Immunology
Aging Research

Background:

Kidney aging causes functional decline, a growing concern for developing anti-aging treatments.
Podocyte injury is a key factor in age-related kidney dysfunction.

Purpose of the Study:

To investigate the role of programmed death-1 (PD-1) in kidney aging.
To explore the therapeutic potential of targeting PD-1 signaling in kidney aging and disease models.

Main Methods:

Unbiased RNA-sequencing (RNA-seq) to identify gene expression changes in aged mouse podocytes.
In vitro studies using immortalized mouse podocytes to assess the effects of PD-1 overexpression.
In vivo studies using aged mice and a mouse model of focal segmental glomerulosclerosis (FSGS) treated with anti-PD-1 antibodies.

Main Results:

PD-1 was found to be upregulated in aged mouse podocytes.
PD-1 overexpression in podocytes led to cell death and a senescence-associated secretory phenotype.
Blocking PD-1 signaling reversed age-related changes in mouse kidneys and reduced proteinuria in an FSGS model.

Conclusions:

Upregulated PD-1 signaling plays a pathological role in aged podocytes.
Targeting PD-1 offers a promising therapeutic strategy for kidney aging and related diseases.
These findings support the potential for PD-1-based therapies in human clinical trials for kidney conditions.