Disease Models, Animal · Journal article

Epigallocatechin-3-gallate attenuates oxidative stress and apoptosis in podocytes of focal segmental glomerulosclerosis.

Renal Failure · August 24, 2026

Hypothesis-Generating Why this matters to you Expert discussion

Raises a question worth testing. It does not answer one.

AI Summary

This preclinical study used single-nucleus RNA sequencing of human FSGS kidney tissue and an adriamycin-induced nephropathy mouse model to characterize oxidative stress and apoptosis in injured podocytes, then tested whether the natural compound EGCG could attenuate these processes in vivo and in vitro. While EGCG showed antioxidant and anti-apoptotic activity in multiple experimental systems, the work remains mechanistic and exploratory; no human efficacy data, clinical endpoints, or direct comparison to established therapies are presented.

What was studied

Mechanistic study combining single-nucleus RNA sequencing, in vivo mouse model, and in vitro cell culture experiments. Three patients with primary FSGS (renal biopsy); three control patients (non-tumorous renal tissue adjacent to clear cell renal cell carcinoma); adriamycin-induced nephropathy mice; conditionally immortalized mouse podocyte clone 5 cell line.. Intervention: Epigallocatechin-3-gallate (EGCG) treatment in vivo (mouse model) and in vitro (podocyte cells). Compared with: Untreated or control-treated adriamycin-induced nephropathy mice and podocytes; healthy podocytes vs. injured podocytes in snRNA-seq analysis. Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.

Key findings

Single-nucleus RNA sequencing identified a subpopulation of injured podocytes in human FSGS and ADR-nephropathy mice with elevated ROS and apoptotic signatures. EGCG treatment in ADR-treated mice significantly reduced the elevation of urine albumin-to-creatinine ratio and alleviated glomerulosclerosis. EGCG attenuated ADR-induced decrease in reduced glutathione/oxidized glutathione ratio in serum and renal tissues of treated mice.

Safety

No human efficacy or safety data; no direct comparison to standard FSGS therapies (immunosuppression, RAAS blockade, SGLT2 inhibitors).

Who this may help

This work identifies EGCG as a potential adjunctive strategy to protect podocytes in FSGS through antioxidant mechanisms, but is a preclinical hypothesis-generating study. Clinical translation requires controlled trials in FSGS patients with renal function or proteinuria endpoints before recommending use in practice.

Plain-language summary

This is a mechanistic study combining transcriptomic analysis with in vivo and in vitro experiments in animal models and cell lines, demonstrating proof-of-concept for EGCG's antioxidant and anti-apoptotic effects in podocytes but providing no clinical trial evidence or human efficacy data.

Study design

As stated by the source record.

MethodsRenal biopsy specimens from three patients with primary FSGS and three controls underwent snRNA-seq. An adriamycin-induced nephropathy mouse model was used to test EGCG effects in vivo. Conditionally immortalized mouse podocyte clone 5 cells were treated with EGCG in vitro. Differential gene expression and pathway enrichment analyses were performed on snRNA-seq data. Specific dosing, treatment duration, randomization, and blinding not stated in available text.

DesignMechanistic study combining single-nucleus RNA sequencing, in vivo mouse model, and in vitro cell culture experiments

PopulationThree patients with primary FSGS (renal biopsy); three control patients (non-tumorous renal tissue adjacent to clear cell renal cell carcinoma); adriamycin-induced nephropathy mice; conditionally immortalized mouse podocyte clone 5 cell line.

InterventionEpigallocatechin-3-gallate (EGCG) treatment in vivo (mouse model) and in vitro (podocyte cells)

ComparatorUntreated or control-treated adriamycin-induced nephropathy mice and podocytes; healthy podocytes vs. injured podocytes in snRNA-seq analysis

SettingSir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China

Reported figures

Quoted from the source exactly as published.

Human FSGS kidney samples for snRNA-seq3

Control kidney samples for snRNA-seq3

Clinical bottom line

Caveats

Source text truncated; full methods, sample sizes for animal and cell experiments, and complete statistical analyses not provided.
No human efficacy or safety data; no direct comparison to standard FSGS therapies (immunosuppression, RAAS blockade, SGLT2 inhibitors).
Adriamycin-induced nephropathy is a disease model, not primary FSGS; generalizability of findings to other FSGS subtypes unknown.
Magnitude of UACR reduction, glomerulosclerosis improvement, and GSH/GSSG ratio changes not reported as numerical values in text.

Evidence assessment

Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.

Study design

limited

Combines snRNA-seq, ADR-induced nephropathy mouse model, and in vitro podocyte cell line; no randomization or blinding stated.

Directness

limited

Surrogate endpoints (ROS, apoptosis markers, UACR) in mice; no human efficacy data; extrapolation from animal model uncertain.

Consistency

moderate

Findings consistent across snRNA-seq, in vivo mouse, and in vitro cell experiments; but limited independent validation.

Risk of bias

insufficient

Methods section incomplete; no blinding, randomization, or allocation concealment details provided.

Sample adequacy

insufficient

Text truncated; human sample n=3 per group stated; mouse and cell experiment sample sizes not reported.

Source abstract

Focal segmental glomerulosclerosis (FSGS) is a major pathological feature of kidney injury, with limited therapeutic options currently available. This study aims to investigate the core mechanisms of podocyte injury in FSGS and the therapeutic potential of the natural extract epigallocatechin-3-gallate (EGCG). Through single-nucleus RNA sequencing of kidney tissues from patients with primary FSGS and an adriamycin (ADR)-induced nephropathy mouse model, we identified a subpopulation of injured podocytes. We found that damaged podocytes exhibited significantly elevated reactive oxygen species (ROS) levels and increased apoptotic activity compared to healthy podocytes. In animal experiments, EGCG treatment effectively reduced the elevation of the urine albumin-to-creatinine ratio, significantly alleviated glomerulosclerosis, and attenuated the ADR-induced decrease in the reduced glutathione/oxidized glutathione ratio in both serum and renal tissues of ADR-treated mice. Furthermore, in vitro treatment of conditionally immortalized mouse podocyte clone 5 confirmed that EGCG significantly reduced ADR-induced ROS production and apoptosis. These findings suggest that EGCG may provide a promising therapeutic approach for alleviating podocyte injury and mitigating FSGS progression.

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Jianbo QingDisease Models, AnimalDezhao LuXiaoyun ShenXiao Wang