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Published on: January 7, 2013
Single-cell transcriptomics identifies ergothioneine as a mitochondrial protector to prevent AKI-to-CKD progression
Jiaxin Peng1, Jing Chen1, Zhipu Qian1
1Department of Internal Medicine and Geriatrics, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, China.
Plos One
|June 23, 2026
Summary
Ergothioneine (EGT) may protect against kidney disease progression. This study shows EGT improves kidney function and reduces injury by supporting mitochondrial health in acute kidney injury (AKI) to chronic kidney disease (CKD) models.
Area of Science:
- Nephrology
- Mitochondrial Biology
- Pharmacology
Background:
- Acute kidney injury (AKI) can progress to chronic kidney disease (CKD).
- Mitochondrial dysfunction is implicated in AKI-to-CKD transition.
- Ergothioneine (EGT) is an antioxidant with potential renoprotective effects.
Purpose of the Study:
- To investigate the role and mechanism of ergothioneine (EGT) in mitigating AKI progression to CKD.
- To explore EGT's effects on renal function, injury, fibrosis, and mitochondrial homeostasis.
Main Methods:
- Cisplatin-induced AKI mouse model with EGT intervention.
- Histopathological examination and biochemical assays.
- Single-cell RNA sequencing (scRNA-seq) and in vitro cell culture.
Main Results:
- EGT improved renal function parameters and attenuated renal injury and fibrosis.
- scRNA-seq indicated EGT partially normalized mitochondrial gene expression in renal tubular cells.
- EGT reduced reactive oxygen species, preserved mitochondrial membrane potential, and increased ATP levels in vitro.
Conclusions:
- Ergothioneine may attenuate AKI-to-CKD progression by improving mitochondrial homeostasis.
- EGT demonstrates potential as a therapeutic strategy for kidney diseases.
- Further research into EGT's mechanisms and clinical efficacy is warranted.
