Many factors, such as ototoxic drugs, noise and aging stress, can induce apoptosis or necrosis of cochlear hair cells, spiral ganglion neurons, stria vascularis, and even cells in the auditory center. The ability of hair cells and neurons to regenerate is extremely weak, resulting in permanent sensorineural hearing loss. Its pathological process is closely related to DNA cross-linking damage, ROS damage, mitochondrial membrane potential damage, autophagy and apoptosis. Although different ototoxic mechanisms have been studied for many years, details have not been fully elucidated, and finding new signaling pathways and targets will provide new ideas and hope for the prevention and treatment of ototoxicity. Our section wants experimental data and clinical data about ototoxicity, including drug-induced deafness, noise and aging stress-induced deafness.
This Research Topic aims to broaden our knowledge of the precise mechanism of ototoxicity and provide a forum for investigators to share their new discoveries. We welcome studies using cell lines, primary tissue culture, animal models and clinical specimens to address the molecular and cellular mechanisms of ototoxicity.
We encourage submissions of original research articles and review papers addressing, but not limited to, the following subtopics:
- Interactions between the drugs and drug-induced ototoxicity;
- Interactions between aging and aging-induced ototoxicity;
- Interactions between the noise and noise-induced ototoxicity;
- The role of autophagy in hearing dysfunction;
Many factors, such as ototoxic drugs, noise and aging stress, can induce apoptosis or necrosis of cochlear hair cells, spiral ganglion neurons, stria vascularis, and even cells in the auditory center. The ability of hair cells and neurons to regenerate is extremely weak, resulting in permanent sensorineural hearing loss. Its pathological process is closely related to DNA cross-linking damage, ROS damage, mitochondrial membrane potential damage, autophagy and apoptosis. Although different ototoxic mechanisms have been studied for many years, details have not been fully elucidated, and finding new signaling pathways and targets will provide new ideas and hope for the prevention and treatment of ototoxicity. Our section wants experimental data and clinical data about ototoxicity, including drug-induced deafness, noise and aging stress-induced deafness.
This Research Topic aims to broaden our knowledge of the precise mechanism of ototoxicity and provide a forum for investigators to share their new discoveries. We welcome studies using cell lines, primary tissue culture, animal models and clinical specimens to address the molecular and cellular mechanisms of ototoxicity.
We encourage submissions of original research articles and review papers addressing, but not limited to, the following subtopics:
- Interactions between the drugs and drug-induced ototoxicity;
- Interactions between aging and aging-induced ototoxicity;
- Interactions between the noise and noise-induced ototoxicity;
- The role of autophagy in hearing dysfunction;
