Ischemia-Reperfusion Increases TRPM7 Expression in Mouse Retinas

Ischemia is the main cause of cell death in retinal diseases such as vascular occlusions, diabetic retinopathy, glaucoma, or retinopathy of prematurity. Although excitotoxicity is considered the primary mechanism of cell death during an ischemic event, antagonists of glutamatergic receptors have been unsuccessful in clinical trials with patients suffering ischemia or stroke. Our main purpose was to analyze if the transient receptor potential channel 7 (TRPM7) could contribute to retinal dysfunction in retinal pathologies associated with ischemia. By using an experimental model of acute retinal ischemia, we analyzed the changes in retinal function by electroretinography and the changes in retinal morphology by optical coherence tomography (OCT) and OCT-angiography (OCTA). Immunohistochemistry was performed to assess the pattern of TRPM7 and its expression level in the retina. Our results show that ischemia elicited a decrease in retinal responsiveness to light stimuli along with reactive gliosis and a significant increase in the expression of TRPM7 in Muller cells. TRPM7 could emerge as a new drug target to be explored in retinal pathologies associated with ischemia.

Automated summary

This study analyzed the role of transient receptor potential channel 7 (TRPM7) in retinal dysfunction associated with ischemia. Using an experimental model, the researchers observed a decrease in retinal responsiveness to light stimuli, reactive gliosis, and an increase in TRPM7 expression in Muller cells during ischemia. The findings suggest that TRPM7 could be a potential drug target for retinal pathologies related to ischemia.