The molecular mechanisms of action of PPAR-γ agonists in the treatment of corneal alkali burns

被引:30
作者
Zhou, Hongyan [1 ]
Zhang, Wensong [2 ]
Bi, Miaomiao [1 ]
Wu, Jie [1 ]
机构
[1] Jilin Univ, Dept Ophthalmol, China Japan Union Hosp, Changchun 130033, Jilin, Peoples R China
[2] Jilin Univ, Dept Ophthalmol, Hosp 2, 4026 Yatai St, Changchun 130000, Jilin, Peoples R China
关键词
corneal alkali burn; corneal neovascularization; inflammation; peroxisome proliferator-activated receptor-; agonists; ACTIVATED-RECEPTOR-GAMMA; MESENCHYMAL STEM-CELLS; OCULAR SURFACE; KAPPA-B; ENDOTHELIAL-CELLS; IMMUNE-RESPONSE; UP-REGULATION; MOUSE MODEL; IN-VIVO; T-CELLS;
D O I
10.3892/ijmm.2016.2699
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
100103 [病原生物学]; 100218 [急诊医学];
摘要
Corneal alkali burns (CAB) are characterized by injury-induced inflammation, fibrosis and neovascularization (NV), and may lead to blindness. This review evaluates the current knowledge of the molecular mechanisms responsible for CAB. The processes of cytokine production, chemotaxis, inflammatory responses, immune response, cell signal transduction, matrix metalloproteinase production and vascular factors in CAB are discussed. Previous evidence indicates that peroxisome proliferator-activated receptor (PPAR-) agonists suppress immune responses, inflammation, corneal fibrosis and NV. This review also discusses the role of PPAR- as an anti-inflammatory, anti-fibrotic and anti-angiogenic agent in the treatment of CAB, as well as the potential role of PPAR- in the pathological process of CAB. There have been numerous studies evaluating the clinical profiles of CAB, and the aim of this systematic review was to summarize the evidence regarding the treatment of CAB with PPAR- agonists.
引用
收藏
页码:1003 / 1011
页数:9
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