Skip to content
2000
Volume 14, Issue 2
  • ISSN: 1566-5232
  • E-ISSN: 1875-5631

Abstract

Hearing impairment is primarily attributed to inner ear hair cell (HC) defects that subsequently lead to spiral ganglion neuron (SGN) loss. The HC loss cannot be self-repaired because of the HCs’ limited capacity to regenerate in mammals. Atoh1, also known as Math1, Hath1, and Cath1, is a proneural basic helix–loop–helix (bHLH) transcription factor that played a major role in HC differentiation. Atoh1 activity at various developmental stages can sufficiently drive HC differentiation in the cochlea. Recent issues of a certain publication have identified that Atoh1 is essential for inner ear development, such as cell growth, morphogenesis, differentiation, cellular maintenance, and survival. We summarize the new findings in Atoh1 research and identify the mechanisms underlying the role of Atoh1 in HC regeneration to launch the future of Atoh1 therapy.

Loading

Article metrics loading...

/content/journals/cgt/10.2174/1566523214666140310143407
2014-04-01
2024-12-23
Loading full text...

Full text loading...

/content/journals/cgt/10.2174/1566523214666140310143407
Loading
This is a required field
Please enter a valid email address
Approval was a Success
Invalid data
An Error Occurred
Approval was partially successful, following selected items could not be processed due to error
Please enter a valid_number test