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HDAC6: A Key Link Between Mitochondria and Development of Peripheral Neuropathy.
Krystal English1,2, Michelle Craig Barton1,3
1UTHealth Graduate School of Biomedical Sciences, The University of Texas MD Anderson Cancer Center, Houston, TX, United States.
Frontiers in Molecular Neuroscience
|September 17, 2021
Summary
Histone deacetylase 6 (HDAC6) inhibition alleviates peripheral neuropathy and neuropathic pain by improving mitochondrial function. This suggests HDAC6 inhibitors are promising therapeutic agents for nerve damage disorders.
Area of Science:
- Neuroscience
- Mitochondrial Biology
- Pharmacology
Background:
- Peripheral neuropathy and neuropathic pain are significant health concerns.
- Traditional research focuses on ion channels and receptors, but mitochondrial dysfunction is increasingly recognized.
- The role of Class IIb histone deacetylase (HDAC6) in neuropathy is under investigation.
Purpose of the Study:
- To review the connection between peripheral neuropathy, mitochondrial dysfunction, and HDAC6.
- To explore HDAC6 as a potential therapeutic target for neuropathic pain.
Main Methods:
- Review of current literature on HDAC6, mitochondrial dynamics, and peripheral neuropathy.
- Analysis of in vivo and in vitro studies investigating HDAC6 inhibition.
Main Results:
- Mitochondrial dysfunction, including altered transport, metabolism, and dynamics, contributes to neuropathy.
- HDAC6 regulates mitochondrial dynamics and may drive dysfunction in peripheral neuropathy.
- HDAC6 inhibition shows significant potential in alleviating neuropathy and pain in preclinical models.
Conclusions:
- HDAC6 plays a critical role in mediating mitochondrial dysfunction in peripheral neuropathy.
- HDAC6 inhibitors represent a promising therapeutic strategy for peripheral neuropathic disorders.
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