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-rat antibodies after 6- and 12-weeks of insulin treatment. This study has also shown that the TRPM3 gene expression in the rat retina is higher after 12 weeks of insulin treatment, and furthermore, this is accompanied by increased plasma membrane localization of the channel ([@B75]). However, in human diabetic retinas, TRPM3 protein expression was similar in treated and untreated patients ([@B44]).
Other forms of TRPM channels activation have been described in the retina after hyperglycemia, in particular after a few weeks of chronic high glucose levels in perfused retinal explants from rats ([@B64]), mice ([@B75]), and bovines ([@B77]). This has been explained by the altered redox potential caused by higher glucose concentrations in the inner retina due to the greater blood flow ([@B64], [@B75]). Nevertheless, since TRPM3 is mostly expressed in the OPL, the innermost and more metabolically active part of the retina, the increase in TRPM3 mRNA and protein levels in this region might be an appropriate target for delaying or preventing the occurrence of diabetic retinopathy. Furthermore, TRPM3 has been described in neuronal cells of the retina ([@B65]), and this suggests that these cells are also involved in retinopathies. In this regard, TRPM3 expression in the inner retina has been associated with ganglion cells in a rat model of optic nerve transection ([@B64]), and with amacrine cells in the experimental autoimmune encephalomyelitis model of multiple sclerosis ([@B64]). It has also been proposed that TRPM3 is expressed in the photoreceptors of the retina ([@B75]), although this has not been confirmed. The exact role of this channel in these cells remains unknown, although a recent study has suggested that it may control intracellular calcium in photoreceptors ([@B75]).
Concluding Remarks {#s5}
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The clinical manifestations of diabetes such as aldose reductase and PTP1B have been shown to be related to TRPM3. In this way, treatment with the compound and the
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