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Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro
Published on: July 17, 2018
circMettl9 promotes retinal mitochondrial dysfunction and apoptosis via miR-10a-5p/Bcl2l11 pathway
Youpei Wang1, Shiyun Liang2, Zhi-Hao Shen2
1National Clinical Research Center for Ocular Diseases, Eye Hospital, Wenzhou Medical University, Wenzhou, 325027, China.
Abstract:
CircRNAs are critical regulators in retinal neural tissues, yet the functions of most retina-enriched members remain unknown. circMettl9, highly expressed in the mouse retina, shows declining expression during postnatal development. Sustained circMettl9 overexpression in adult retinas via AAV-mediated subretinal injection triggers Müller gliosis, secretion of pro-inflammatory cytokines and retinal functional impairment: elevated GFAP levels and abnormal electroretinogram (ERG) responses were detected, while overt structural abnormalities were absent. Mechanistically, circMettl9 drives mitochondrial dysfunction, oxidative stress elevation and caspase-3 activation to promote retinal cell apoptosis via the circMettl9/miR-10a-5p/Bcl2l11 axis. Our study is the first to clarify the biological role of circMettl9 in mouse retina, providing novel theoretical insights and potential therapeutic targets for retinal diseases.
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