Accumulated ROS Activates HIF-1α-Induced Glycolysis and Exerts a Protective Effect on Sensory Hair Cells Against Noise-Induced Damage

• DOI: 10.3389/fmolb.2021.806650
• Publication Date: 2022-01-12T18:43:33Z
• Authors: Shuo Liang; Shuohui Dong; Wenwen Liu; Man Wang; Shanshan Tian; Yu Ai; Haibo Wang
• Keywords: Mitochondrial ROS

Noise exposure causes noise-induced hearing loss (NIHL). NIHL exhibits of inner ear sensory hair cells and is often irreparable. Although oxidative stress involved in loss, the complex mechanisms are unclear. Hypoxia-inducible factor 1α (HIF-1α) has been suggested to be essential for protecting cells. Additionally, it shown that ROS modulating stability HIF-1α. To investigate pathogenesis, we established a tert-butyl hydroperoxide (t-BHP)-induced damage model hair-like HEI-OC1 an C57BL/6 mice. Protein mRNA expression were determined, biochemical parameters including reactive oxygen species (ROS) accumulation, glucose uptake, adenosine triphosphat (ATP) production, mitochondrial content evaluated. In cells, t-BHP induced accumulation reduced consumption, but ATP level was unaffected. there increased uptake lactate release along with elevated HIF-1α, transporter 1, several glycolytic enzymes. Consistently, noise trauma HIF-1α enzymes Thus, concluded expression, which promoted glycolysis, suggesting metabolic shift maintained attenuate cell NIHL.