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. 2015 Sep 10;6(9):e1882.
doi: 10.1038/cddis.2015.252.

Preventing ototoxic hearing loss by inhibiting histone deacetylases

W S Layman  1 , J Zuo  1
Affiliations

Preventing ototoxic hearing loss by inhibiting histone deacetylases

W S Layman et al. Cell Death Dis. .
No abstract available

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Figures

Figure 1
Figure 1
A simplified schematic diagram depicting aminoglycoside-induced hair cell death in the mammalian inner ear. Aminoglycoside exposure causes reactive oxygen species (ROS), stress kinases, and the caspase family of proteases to become activated in hair cells. Histone deacetylase (HDAC) inhibition using suberoylanilide hydroxamic acid (SAHA) stops the HDAC-mediated deacetylation of pro-survival transcription factors RelA (Nf-κB), Sp1, and Foxo3a. Blocking the deacetylation of RelA K310 results in transcriptional activation of pro-survival genes Cflar (cFLIP) and Bcl2l1 (Bcl-xL), which impedes aminoglycoside-induced apoptotic cell death. SAHA also inhibits Sp1 and Foxo3a deacetylation causing an increase in expression of pro-survival genes Cdkn1a (p21CIP1) and Hspa1a (Hsp70). Abbreviations: c-Jun N-terminal kinase (JNK)
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