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Methylglyoxal: A Key Factor for Diabetic Retinopathy and Its Effects on Retinal Damage
被引:1
|作者:
Klochkov, Vladlen
[1
,2
]
Chan, Chi-Ming
[2
,3
]
Lin, Wan-Wan
[1
,4
]
机构:
[1] Taipei Med Univ, Grad Inst Med Sci, Taipei 11031, Taiwan
[2] Cardinal Tien Hosp, Dept Ophthalmol, New Taipei City 23148, Taiwan
[3] Fu Jen Catholic Univ, Sch Med, New Taipei City 242062, Taiwan
[4] Natl Taiwan Univ, Coll Med, Dept Pharmacol, Taipei 100233, Taiwan
关键词:
methylglyoxal;
diabetic retinopathy;
oxidative stress;
inflammation;
autophagy;
ER stress;
glyoxalase;
GLYCATION END-PRODUCTS;
ENDOTHELIAL GROWTH-FACTOR;
PIGMENT EPITHELIAL-CELLS;
OXIDATIVE STRESS;
GLYOXALASE;
INDUCED CYTOTOXICITY;
GLUCOSE METABOLITE;
SIGNALING PATHWAY;
IN-VITRO;
KAPPA-B;
D O I:
10.3390/biomedicines12112512
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
Background: Diabetic retinopathy is the most common retinal vascular disease, affecting the retina's blood vessels and causing chronic inflammation, oxidative stress, and, ultimately, vision loss. Diabetes-induced elevated glucose levels increase glycolysis, the main methylglyoxal (MGO) formation pathway. MGO is a highly reactive dicarbonyl and the most rapid glycation compound to form endogenous advanced glycation end products (AGEs). MGO can act both intra- and extracellularly by glycating molecules and activating the receptor for AGEs (RAGE) pathway. Conclusions: This review summarizes the sources of MGO formation and its actions on various cell pathways in retinal cells such as oxidative stress, glycation, autophagy, ER stress, and mitochondrial dysfunction. Finally, the detoxification of MGO by glyoxalases is discussed.
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页数:17
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