1990
DOI: 10.1001/archopht.1990.01070140118041
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Inflammatory Mediators in Postoperative Aphakic and Pseudophakic Baboon Eyes

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Cited by 59 publications
(33 citation statements)
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“…Meanwhile, other risks of topical steroids have become known, such as elevation of intraocular pressure, activation of ocular infection, worsening of viral infection and the development of cataract itself [6, 7, 8, 9, 10]. A better understanding of ocular and postsurgical inflammation, especially the breakdown of cell membrane phospholipids and the inhibitory potency of nonsteroidal anti-inflammatory substances, brought these drugs (NSAIDs) into the field of interest [11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24]. …”
Section: Introductionmentioning
confidence: 99%
“…Meanwhile, other risks of topical steroids have become known, such as elevation of intraocular pressure, activation of ocular infection, worsening of viral infection and the development of cataract itself [6, 7, 8, 9, 10]. A better understanding of ocular and postsurgical inflammation, especially the breakdown of cell membrane phospholipids and the inhibitory potency of nonsteroidal anti-inflammatory substances, brought these drugs (NSAIDs) into the field of interest [11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24]. …”
Section: Introductionmentioning
confidence: 99%
“…It has been reported that the cause of CME is multifactorial including the release of bioactive substances such as prostaglandins, cytokines, and growth factors following cataract surgery [12][13][14] . We therefore proposed that the onset of CME after cataract surgery may relate to oxidative stress in the retina due to the following : 1 the retina absorbs short wavelength UV and blue light leading to a photochemical reaction that generates reactive oxygen species ROS 15 , and resultant oxidative stress ; 2 ROS activate transcription factors, such as nuclear factor kappa B 16 and mitogen-activated protein kinase MAPK , and thereby increase cycloxygenase-2 activity ; 3 these transcription factors then upregulate the cytokines, vascular endothelial growth factor VEGF 17 and interleukin-1 beta IL-1 beta 18 , as well as prostaglandins in the retina ; and then, 4 these biologically active compounds disrupt the tight junctions by inhibiting de novo synthesis of the required component proteins, leading to macular edema 19,20 Gass et al 1 showed regression of edema in 50% of CME patients 6 months after cataract surgery and in 20% of patients between 1 and 3 years, with 30% of patients showing no improvement in 3 or more years.…”
Section: Discussionmentioning
confidence: 99%
“…Although the major form of TGF-ß present in the normal aqueous humor is TGF-ß 2 [10], it is possible that an isoform such as TGF-ß 1 or TGF-ß 3 contributes to gel contraction. In addition, a variety of chemical mediators and cytokines are involved in the inflammation following cataract surgery [29]. The contraction of the collagen gels depends on matrix remodeling [30].…”
Section: Discussionmentioning
confidence: 99%