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Oxidative Stress-Related Mechanisms and Antioxidant Therapy in Diabetic Retinopathy.

Abstract Diabetic retinopathy (DR) is one of the most common microvascular complications of diabetes and is the leading cause of blindness in young adults. Oxidative stress has been implicated as a critical cause of DR. Metabolic abnormalities induced by high-glucose levels are involved in the development of DR and appear to be influenced by oxidative stress. The imbalance between reactive oxygen species (ROS) production and the antioxidant defense system activates several oxidative stress-related mechanisms that promote the pathogenesis of DR. The damage caused by oxidative stress persists for a considerable time, even after the blood glucose concentration has returned to a normal level. Animal experiments have proved that the use of antioxidants is a beneficial therapeutic strategy for the treatment of DR, but more data are required from clinical trials. The aims of this review are to highlight the improvements to our understanding of the oxidative stress-related mechanisms underlying the development of DR and provide a summary of the main antioxidant therapy strategies used to treat the disease.
PMID
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Authors

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




PMID- 28265339
OWN - NLM
STAT- MEDLINE
DA  - 20170307
DCOM- 20170313
LR  - 20170313
IS  - 1942-0994 (Electronic)
IS  - 1942-0994 (Linking)
VI  - 2017
DP  - 2017
TI  - Oxidative Stress-Related Mechanisms and Antioxidant Therapy in Diabetic
      Retinopathy.
PG  - 9702820
LID - 10.1155/2017/9702820 [doi]
AB  - Diabetic retinopathy (DR) is one of the most common microvascular complications
      of diabetes and is the leading cause of blindness in young adults. Oxidative
      stress has been implicated as a critical cause of DR. Metabolic abnormalities
      induced by high-glucose levels are involved in the development of DR and appear
      to be influenced by oxidative stress. The imbalance between reactive oxygen
      species (ROS) production and the antioxidant defense system activates several
      oxidative stress-related mechanisms that promote the pathogenesis of DR. The
      damage caused by oxidative stress persists for a considerable time, even after
      the blood glucose concentration has returned to a normal level. Animal
      experiments have proved that the use of antioxidants is a beneficial therapeutic 
      strategy for the treatment of DR, but more data are required from clinical
      trials. The aims of this review are to highlight the improvements to our
      understanding of the oxidative stress-related mechanisms underlying the
      development of DR and provide a summary of the main antioxidant therapy
      strategies used to treat the disease.
FAU - Li, Cheng
AU  - Li C
AUID- ORCID: 0000-0003-2439-1627
AD  - The First Hospital of Jilin University, Changchun 130021, China.
FAU - Miao, Xiao
AU  - Miao X
AD  - The Second Hospital of Jilin University, Changchun 130041, China.
FAU - Li, Fengsheng
AU  - Li F
AUID- ORCID: 0000-0001-5051-9669
AD  - General Hospital of the PLA Rocket Force, Beijing 100088, China.
FAU - Wang, Shudong
AU  - Wang S
AUID- ORCID: 0000-0003-2017-8968
AD  - The First Hospital of Jilin University, Changchun 130021, China.
FAU - Liu, Quan
AU  - Liu Q
AUID- ORCID: 0000-0001-7408-0048
AD  - The First Hospital of Jilin University, Changchun 130021, China.
FAU - Wang, Yonggang
AU  - Wang Y
AUID- ORCID: 0000-0003-0370-4591
AD  - The First Hospital of Jilin University, Changchun 130021, China.
FAU - Sun, Jian
AU  - Sun J
AUID- ORCID: 0000-0002-4257-8674
AD  - The First Hospital of Jilin University, Changchun 130021, China.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20170206
PL  - United States
TA  - Oxid Med Cell Longev
JT  - Oxidative medicine and cellular longevity
JID - 101479826
RN  - 0 (Antioxidants)
SB  - IM
MH  - Animals
MH  - Antioxidants/*pharmacology
MH  - Diabetic Retinopathy/*drug therapy
MH  - Humans
MH  - Oxidative Stress/*drug effects
PMC - PMC5317113
COI - The authors declare that there is no conflict of interests regarding the
      publication of this paper.
EDAT- 2017/03/08 06:00
MHDA- 2017/03/14 06:00
CRDT- 2017/03/08 06:00
PHST- 2016/10/14 [received]
PHST- 2016/11/27 [revised]
PHST- 2016/12/27 [accepted]
AID - 10.1155/2017/9702820 [doi]
PST - ppublish
SO  - Oxid Med Cell Longev. 2017;2017:9702820. doi: 10.1155/2017/9702820. Epub 2017 Feb
      6.

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