# FAK mediates noise-induced loss of auditory hair cell function and survival

> **NIH NIH R21** · OREGON HEALTH & SCIENCE UNIVERSITY · 2022 · $231,000

## Abstract

Project Summary
Mitochondrial dysfunction has long been recognized as an underlying mechanism of noise-induced loss of
hearing sensitivity (NIHL). However, the initiating processes that lead to this dysfunction is poorly understood.
This proposal is founded upon new and important findings involving changes in mitochondrial dynamics in outer
hair cells after loud sound exposure. Mitochondria are highly dynamic organelles that constantly undergo fission
and fusion to adapt to changes in the cellular environment, and it is becoming increasingly clear that
mitochondrial morphology is directly related to mitochondrial function and, therefore, the health and survival of
the cell. The studies proposed here will examine a potential integrin signaling pathway for induction of
mitochondrial fission activity. Specifically, we will investigate the role of FAK as a mediator of noise-induced
overstimulation of OHCs leading to cell death and loss of hearing sensitivity.

## Key facts

- **NIH application ID:** 10527266
- **Project number:** 1R21DC019756-01A1
- **Recipient organization:** OREGON HEALTH & SCIENCE UNIVERSITY
- **Principal Investigator:** ALFRED L NUTTALL
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $231,000
- **Award type:** 1
- **Project period:** 2022-06-03 → 2024-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10527266

## Citation

> US National Institutes of Health, RePORTER application 10527266, FAK mediates noise-induced loss of auditory hair cell function and survival (1R21DC019756-01A1). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/10527266. Licensed CC0.

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