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Oxidative Stress and Cataractogenesis

Call for Papers

A cataract is a clouding of the eye's natural lens, which lies behind the iris and the pupil. More precisely, it is the opacification of eye lens, associated with the breakdown of the eye lens protein microarchitecture, adversely affecting the transmission of light onto the retina. Cataract remains the leading cause of blindness worldwide. The age-related cataract accounts for approximately 50% of blindness worldwide. In developing countries, 50–90% of all blindness is caused by cataracts. Apart from ageing, diabetes has been attributed as major risk factor of cataractogenesis. The high sugar levels in diabetes may cause tissue disruption and intumescences by osmotic changes induced via aldose reductase mediated polyol pathway. Thus, a contribution of polyol pathway to oxidative stress (OS) in diabetic cataract is a well-established fact. Moreover, glycation of lens proteins results in the formation of advanced glycation end products (AGEs) which contribute to the generation of oxidative stress and thereby implicates in the cataractogenesis. Plethora of scientific evidence has accumulated in the recent past linking the role of OS and ROS in cataractogenesis. Biochemical evidence demonstrates that the oxidative damage of the lens proteins is involved in the genesis of age-related cataract. In particular, the lens proteins are subjected to extensive oxidative modifications. The lens epithelium cell is the center of metabolic activities in lenses, and oxidative damage to LECs plays a significant role in the pathogenesis of many forms of cataracts. The pathophysiology of OS/ROS induced causation of cataract has remained a major thrust area in the mainstream of cataract research.

We invite authors to contribute original research articles as well as review articles that encourage continuing endeavors to clear not only the pathophysiology of cataractogenesis in the light of oxidative stress but also expand the knowledge and strategies to treat or prevent the process of cataractogenesis targeting the OS/ROS. New findings on the role of oxidative stress in initiation and development of cataract are welcome. Potential topics include, but are not limited to:

  • Recent molecular investigations describing the pathophysiology of cataractogenesis in the light of OS/ROS
  • Novel inhibitors for arresting AR activity, glycation of lens proteins, aggregation of lens proteins AGEs, and molecular mechanisms involved therein
  • Molecular mechanisms of interventions of antioxidants in age-related and diabetic cataract formation
  • Novel methods for analysis of OS/ROS load during cataractogenesis
  • Molecular mechanisms of dietary polyphenols/flavonoids/other phytochemicals targeting the OS/ROS implicated in cataract formation
  • Novel drug discoveries targeting OS/ROS mediated cataract formation

Before submission authors should carefully read over the journal’s Author Guidelines which are located at http://www.hindawi.com/journals/omcl/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/submit/journals/omcl/scat/ according to the following timetable:

Manuscript DueFriday, 28 March 2014
First Round of ReviewsFriday, 20 June 2014
Publication DateFriday, 15 August 2014

Lead Guest Editor

  • Rajesh N. Gacche, School of Life Sciences, S. R. T. M. University, Nanded, Maharashtra, India

Guest Editors