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Editors Selection IGR 21-3

Basic research: IOP: circadian rhythm

John Liu

Comment by John Liu on:

14031 Circadian intraocular pressure rhythm is generated by clock genes, Maeda A; Tsujiya S; Higashide T et al., Investigative Ophthalmology and Visual Science, 2006; 47: 4050-4052


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There is a circadian (24-hour) rhythm in intraocular pressure (IOP) in humans and in various animal species. Whether the appearance of this circadian IOP rhythm is due mainly to genetic influence or environmental influence has been less clear. Recent studies into the molecular mechanisms of the circadian clock have identified 2 cry genes and 3 per genes as constituting the primary machinery in the feedback loop regulating circadian rhythms in mammals. Knockout of both the cry1 and cry2 genes in the common C57BL/6 mouse strain yielded mice without circadian rhythms in locomotive activity and in body temperature. Maeda et al. (708) have presented clear evidence that these cry-deficient mice do not have a circadian IOP rhythm.

For the first time, a genetic component related to the circadian rhythm of IOP has been identified
For the first time, a genetic component related to the circadian rhythm of IOP has been identified. In the mammalian body, initial signals for circadian rhythms are generated by clock genes in the cells of the suprachiasmatic nucleus in the hypothalamus. In order to synchronize the biological rhythms with the environmental light-dark conditions, cells in the suprachiasmatic nucleus adjust their circadian signals using the neural inputs from the retinal ganglion cells that sense the environmental illumination indirectly and, in some species, directly. The hallmark of glaucomatous damage is the loss of retinal ganglion cells. It is possible that a significant loss of retinal ganglion cells in glaucoma can impair the ability of the suprachiasmatic nucleus to synchronize circadian rhythms with the environmental light-dark conditions. This interference may affect the 24-hour pattern of IOP in patients with advanced glaucoma. Ironically, an abnormal IOP is a significant risk factor for the progression of glaucoma. The impact of a significant loss in retinal ganglion cells on the 24-hour control of IOP in advanced glaucoma patients is unknown. Further research is warranted, which may have significant clinical implications.

(See also introduction: More than the eye)



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