Zhang Xu

Ying Qian, Luo Hongdou, Xie Zhi, Huang Yi, Hu Haijian, Jin Ming et al.

SIRT4 protects the retina from excitotoxic injury by promoting Müller cell mitochondrial fusion and GLAST expression, offering a potential therapeutic target for retinal diseases.

Li Jiayong, Ma Xin, Zhuo Kaichen, He Yuxian, Lin Mingkai, Wang Wei et al.

This genetic study found no definitive causal link between gut microbiota and glaucoma, despite some associations. Clinical relevance: Gut-eye axis in glaucoma is complex, requiring cautious interpretation and further research.

Xie Zhi, Ying Qian, Luo Hongdou, Qin Mengqi, Pang Yulian, Hu Haijian et al.

Resveratrol reduced retinal damage and ganglion cell death in ischemia-reperfusion injury by inhibiting the NLRP3/Gasdermin D pyroptosis pathway, suggesting a neuroprotective therapeutic strategy for glaucoma.

Luo Hongdou, Zhuang Jiejie, Hu Piaopiao, Ye Wei, Chen Shanshan, Pang Yulian et al.

Resveratrol protected retinal ganglion cells and reduced inflammation/gliosis in a glaucoma model, suggesting it could be a therapeutic strategy for glaucoma.

Mi Xue-Song, Zhang Xu, Feng Qian, Lo Amy Cheuk Yin, Chung Sookja Kim, So Kwok-Fai

Mice overexpressing vascular ET-1 developed progressive retinal degeneration, including RGC loss and retinal thinning, despite normal IOP, suggesting a model for vascular-associated retinal diseases like normal tension glaucoma.

Zhang Xu, Sun Peng, Wang Jian, Wang Qing, Song Sheng-Kwei

DTI detected early RGC axon damage in a mouse glaucoma model, showing promise as a non-invasive tool for assessing axonal injury progression, potentially aiding early glaucoma diagnosis.

Zhang Xu, Neufeld Arthur H

Activating EGFR in optic nerve astrocytes rapidly induces COX-2 and inflammatory PGE2 release. This early signaling could indicate neural damage, suggesting potential therapeutic targets in glaucoma.

Zhang Xu, Cheng Mei, Chintala Shravan K

Kainic acid increased retinal MMP-9, causing ganglion cell loss and degeneration. Inhibiting MMP-9 or non-NMDA receptors protected against this damage, suggesting new therapeutic targets for excitotoxic retinal diseases.