# Novel mechanisms of redox signaling in acute kidney injury

> **NIH NIH K01** · UT SOUTHWESTERN MEDICAL CENTER · 2021 · $149,035

## Abstract

PROJECT SUMMARY
Acute kidney injury resulting from ischemia reperfusion or toxin induced damage is correlated with mitochondrial
dysfunction and increased ROS levels. The damaging effects of ROS on DNA, protein and lipids can be
ameliorated by cellular antioxidants that detoxify the ROS. I have identified a novel mechanism of cellular
detoxification in the mitochondria by a predicted pseudokinase, Selenoprotein O (SelO). Preliminary studies
using E. coli and S. cerevisiae demonstrates that SelO catalyzes the transfer of AMP from ATP to multiple
substrates involved in redox homeostasis to dampen oxidative damage and prevent cell death. Due to the
phyletic spread and conservation from bacteria to humans, we postulate that SelO will play a role in oxidative
stress response in mammalian systems that are heavily dependent on the mitochondria, such as the kidney. We
will test this hypothesis by identifying the molecular targets and pathways mediated by SelO, and characterizing
the functional importance of SelO in the rodent cisplatin-induced acute kidney injury model. A deep
understanding and technical expertise in the fields of oxidative stress and nephrology are essential to the
successful completion of this proposal. This career development award will allow me to strengthen my scientific
skill set by training in kidney isolation, staining and phenotypic characterization in combination with biochemical
assays to evaluate mitochondrial health. These studies will define a novel paradigm of signaling in the
mitochondria, which can be usurped to identify therapeutic targets to prevent oxidative damage in a plethora of
pathologies including acute kidney injury.

## Key facts

- **NIH application ID:** 10092155
- **Project number:** 5K01DK123194-02
- **Recipient organization:** UT SOUTHWESTERN MEDICAL CENTER
- **Principal Investigator:** Anju Sreelatha
- **Activity code:** K01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $149,035
- **Award type:** 5
- **Project period:** 2020-02-01 → 2024-01-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10092155

## Citation

> US National Institutes of Health, RePORTER application 10092155, Novel mechanisms of redox signaling in acute kidney injury (5K01DK123194-02). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10092155. Licensed CC0.

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