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Published on: November 21, 2025
Oxidative stress and autophagy: crucial modulators of kidney injury
Angara Sureshbabu1, Stefan W Ryter1, Mary E Choi1
1Joan and Sanford I. Weill Department of Medicine, New York-Presbyterian Hospital, Weill Cornell Medical College, New York, NY, USA.
Abstract:
Both acute kidney injury (AKI) and chronic kidney disease (CKD) that lead to diminished kidney function are interdependent risk factors for increased mortality. If untreated over time, end stage renal disease (ESRD) is an inevitable outcome. Acute and chronic kidney diseases occur partly due to imbalance between the molecular mechanisms that govern oxidative stress, inflammation, autophagy and cell death. Oxidative stress refers to the cumulative effects of highly reactive oxidizing molecules that cause cellular damage. Autophagy removes damaged organelles, protein aggregates and pathogens by recruiting these substrates into double membrane vesicles called autophagosomes which subsequently fuse with lysosomes. Mounting evidence suggests that both oxidative stress and autophagy are significantly involved in kidney health and disease. However, very little is known about the signaling processes that link them. This review is focused on understanding the role of oxidative stress and autophagy in kidney diseases. In this review, we also discuss the potential relationships between oxidative stress and autophagy that may enable the development of better therapeutic intervention to halt the progression of kidney disease and promote its repair and resolution.
Insights
Oxidative stress and autophagy are key players in kidney disease progression. Understanding their interplay may lead to new therapies for kidney repair and halting disease advancement.
Area of Science:
- Nephrology
- Molecular Biology
- Cellular Biology
Background:
- Acute kidney injury (AKI) and chronic kidney disease (CKD) are interdependent, increasing mortality and potentially leading to end-stage renal disease (ESRD).
- Kidney diseases arise partly from an imbalance in molecular mechanisms including oxidative stress, inflammation, autophagy, and cell death.
- Oxidative stress involves cellular damage from reactive oxidizing molecules, while autophagy removes damaged cellular components via autophagosomes.
Purpose of the Study:
- To review the roles of oxidative stress and autophagy in kidney diseases.
- To explore the signaling pathways linking oxidative stress and autophagy.
- To identify potential therapeutic interventions for kidney disease based on these mechanisms.
Main Methods:
- Literature review of existing research on oxidative stress, autophagy, and kidney disease.
- Analysis of molecular mechanisms and signaling pathways involved.
- Synthesis of findings to propose therapeutic strategies.
Main Results:
- Both oxidative stress and autophagy are significantly implicated in kidney health and disease.
- Evidence suggests a complex relationship between oxidative stress and autophagy in the kidney.
- Specific signaling pathways linking these processes are not yet fully elucidated.
Conclusions:
- Further research into the crosstalk between oxidative stress and autophagy is crucial for developing effective kidney disease treatments.
- Targeting these pathways may offer novel therapeutic avenues to halt disease progression and promote kidney repair.
- A deeper understanding can lead to interventions that improve outcomes for patients with AKI and CKD.
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