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Targeting Oxidative Stress for Treatment of Glaucoma and Optic Neuritis.

Abstract Glaucoma is a neurodegenerative disease of the eye and it is one of the leading causes of blindness. Glaucoma is characterized by progressive degeneration of retinal ganglion cells (RGCs) and their axons, namely, the optic nerve, usually associated with elevated intraocular pressure (IOP). Current glaucoma therapies target reduction of IOP, but since RGC death is the cause of irreversible vision loss, neuroprotection may be an effective strategy for glaucoma treatment. One of the risk factors for glaucoma is increased oxidative stress, and drugs with antioxidative properties including valproic acid and spermidine, as well as inhibition of apoptosis signal-regulating kinase 1, an enzyme that is involved in oxidative stress, have been reported to prevent glaucomatous retinal degeneration in mouse models of glaucoma. Optic neuritis is a demyelinating inflammation of the optic nerve that presents with visual impairment and it is commonly associated with multiple sclerosis, a chronic demyelinating disease of the central nervous system. Although steroids are commonly used for treatment of optic neuritis, reduction of oxidative stress by approaches such as gene therapy is effective in ameliorating optic nerve demyelination in preclinical studies. In this review, we discuss oxidative stress as a therapeutic target for glaucoma and optic neuritis.
PMID
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Authors

Mayor MeshTerms
Keywords
Journal Title oxidative medicine and cellular longevity
Publication Year Start




PMID- 28270908
OWN - NLM
STAT- MEDLINE
DA  - 20170308
DCOM- 20170313
LR  - 20170313
IS  - 1942-0994 (Electronic)
IS  - 1942-0994 (Linking)
VI  - 2017
DP  - 2017
TI  - Targeting Oxidative Stress for Treatment of Glaucoma and Optic Neuritis.
PG  - 2817252
LID - 10.1155/2017/2817252 [doi]
AB  - Glaucoma is a neurodegenerative disease of the eye and it is one of the leading
      causes of blindness. Glaucoma is characterized by progressive degeneration of
      retinal ganglion cells (RGCs) and their axons, namely, the optic nerve, usually
      associated with elevated intraocular pressure (IOP). Current glaucoma therapies
      target reduction of IOP, but since RGC death is the cause of irreversible vision 
      loss, neuroprotection may be an effective strategy for glaucoma treatment. One of
      the risk factors for glaucoma is increased oxidative stress, and drugs with
      antioxidative properties including valproic acid and spermidine, as well as
      inhibition of apoptosis signal-regulating kinase 1, an enzyme that is involved in
      oxidative stress, have been reported to prevent glaucomatous retinal degeneration
      in mouse models of glaucoma. Optic neuritis is a demyelinating inflammation of
      the optic nerve that presents with visual impairment and it is commonly
      associated with multiple sclerosis, a chronic demyelinating disease of the
      central nervous system. Although steroids are commonly used for treatment of
      optic neuritis, reduction of oxidative stress by approaches such as gene therapy 
      is effective in ameliorating optic nerve demyelination in preclinical studies. In
      this review, we discuss oxidative stress as a therapeutic target for glaucoma and
      optic neuritis.
FAU - Kimura, Atsuko
AU  - Kimura A
AD  - Visual Research Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, 
      Japan.
FAU - Namekata, Kazuhiko
AU  - Namekata K
AD  - Visual Research Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, 
      Japan.
FAU - Guo, Xiaoli
AU  - Guo X
AD  - Visual Research Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, 
      Japan.
FAU - Noro, Takahiko
AU  - Noro T
AD  - Visual Research Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, 
      Japan.
FAU - Harada, Chikako
AU  - Harada C
AD  - Visual Research Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, 
      Japan.
FAU - Harada, Takayuki
AU  - Harada T
AUID- ORCID: 0000-0001-6167-0997
AD  - Visual Research Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, 
      Japan.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20170208
PL  - United States
TA  - Oxid Med Cell Longev
JT  - Oxidative medicine and cellular longevity
JID - 101479826
SB  - IM
MH  - Animals
MH  - Glaucoma/*therapy
MH  - Humans
MH  - Optic Neuritis/*therapy
MH  - Oxidative Stress/*physiology
PMC - PMC5320364
COI - The authors declare that there is no conflict of interests regarding the
      publication of this manuscript.
EDAT- 2017/03/09 06:00
MHDA- 2017/03/14 06:00
CRDT- 2017/03/09 06:00
PHST- 2016/12/02 [received]
PHST- 2017/01/09 [accepted]
AID - 10.1155/2017/2817252 [doi]
PST - ppublish
SO  - Oxid Med Cell Longev. 2017;2017:2817252. doi: 10.1155/2017/2817252. Epub 2017 Feb
      8.

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