Neural Regeneration Research · 10 authors, 2 centres
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In a mouse model and in vitro experiments, the study found that the short-form Homer1 protein (Homer1a) reduced inflammation and cell death following retinal ischemia/reperfusion injury, acting via the caspase-8/NF-κB/NLRP3 signaling pathway.
This preclinical study used a mouse model of retinal ischemia/reperfusion (I/R) injury and in vitro Müller cell cultures to investigate the protective role of Homer1a. Methods included I/R injury induction, Homer1a manipulation via viral vectors, and analysis of retinal thickness, apoptosis, and inflammatory pathways. Overexpression of Homer1a improved Müller cell viability, reduced apoptosis, and inhibited inflammatory factors like IL-1β and IL-18. Mechanistically, Homer1a knockdown promoted caspase-8 activation of NF-κB p65, NLRP3 inflammasome formation, and cytokine processing, effects reversed by Homer1a overexpression. Combined Homer1a protein and JSH-23 treatment improved retinal thickness and reduced apoptosis. Limitations include uncertainty about the specific retinal cell types targeted by Homer1a in vivo. The findings suggest Homer1a mitigates inflammation after retinal I/R via the caspase-8/NF-κB/NLRP3 pathway, offering potential therapeutic insights for retinal diseases.
