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ShareNov. 30, 2009 — A group led by Dr. Jian-xing Ma at The University of Oklahoma Health Sciences Center, Oklahoma City, OK has demonstrated that the Wnt signaling pathway plays a role in diabetic retinopathy. Their report can be found in the December 2009 issue of The American Journal of Pathology.
Diabetic retinopathy, damage to the retina in the eye as a result of inflammatory complications of diabetes mellitus, affects up to 80% of all patients who have had diabetes for 10 years or more. Diabetic retinopathy is the leading cause of blindness in the working age population; however, the mechanisms by which diabetes induces this inflammation remain unclear.
To determine if the Wnt signaling pathway, which is activated under numerous pathological conditions, plays a role in diabetic retinopathy, Chen et al examined retinal expression and activation of a Wnt signaling molecule in human patients with diabetic retinopathy as well as in mouse models. They found high retinal expression and activation of Wnt signaling molecules in patients with diabetic retinopathy. Moreover, blocking Wnt signaling decreased the severity of diabetic retinopathy in mouse models. Wnt therefore provides a new target for diabetic retinopathy therapy.
Taken together, the data by Dr. Ma and colleagues suggest that "Wnt pathway activation is a novel pathogenic mechanism for [diabetic retinopathy] in both human patients and in animal models. Thus, the Wnt pathway represents a new target for pharmaceutical intervention of [diabetic retinopathy]."
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The above story is reprinted from materials provided by American Journal of Pathology, via EurekAlert!, a service of AAAS.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
- Chen et al. Activation of the Wnt Pathway Plays a Pathogenic Role in Diabetic Retinopathy in Humans and Animal Models. American Journal Of Pathology, 2009; DOI: 10.2353/ajpath.2009.080945
Note: If no author is given, the source is cited instead.
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