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Molecular regulation of auditory hair cell death and approaches to protect sensory receptor cells and/or stimulate repair following acoustic trauma

Overview of attention for article published in Frontiers in Cellular Neuroscience, March 2015
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Title
Molecular regulation of auditory hair cell death and approaches to protect sensory receptor cells and/or stimulate repair following acoustic trauma
Published in
Frontiers in Cellular Neuroscience, March 2015
DOI 10.3389/fncel.2015.00096
Pubmed ID
Authors

Christine T. Dinh, Stefania Goncalves, Esperanza Bas, Thomas R. Van De Water, Azel Zine

Abstract

Loss of auditory sensory hair cells (HCs) is the most common cause of hearing loss. This review addresses the signaling pathways that are involved in the programmed and necrotic cell death of auditory HCs that occur in response to ototoxic and traumatic stressor events. The roles of inflammatory processes, oxidative stress, mitochondrial damage, cell death receptors, members of the mitogen-activated protein kinase (MAPK) signal pathway and pro- and anti-cell death members of the Bcl-2 family are explored. The molecular interaction of these signal pathways that initiates the loss of auditory HCs following acoustic trauma is covered and possible therapeutic interventions that may protect these sensory HCs from loss via apoptotic or non-apoptotic cell death are explored.

Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 97 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Germany 1 1%
Unknown 96 99%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 19 20%
Researcher 17 18%
Student > Master 13 13%
Student > Bachelor 8 8%
Other 7 7%
Other 16 16%
Unknown 17 18%
Readers by discipline Count As %
Neuroscience 17 18%
Medicine and Dentistry 17 18%
Biochemistry, Genetics and Molecular Biology 14 14%
Agricultural and Biological Sciences 12 12%
Engineering 4 4%
Other 12 12%
Unknown 21 22%