Li Guorong

Kim Daniel, Fang Raymond, Zhang Pengpeng, Yan Zihang, Sun Cheng, Li Guorong et al.

Mouse eye chamber volumes were quantified, revealing the posterior chamber is larger than the anterior, unlike humans. This finding necessitates reassessing mouse aqueous humor dynamics and inflow rate estimates.

Li Guorong, Nottebaum Astrid F, Brigell Mitchell, Navarro Iris D, Ipe Ute, Mishra Sarthak et al.

A Tie2 activator (AKB-9778) was studied for glaucoma. It lowered human and animal IOP by activating Tie2 in Schlemm's canal, increasing outflow. This offers a new glaucoma treatment approach.

De Ieso Michael L, Gurley Jami M, McClellan Mark E, Gu Xiaowu, Navarro Iris, Li Guorong et al.

Targeting endothelial Cav1 in mice elevated eye pressure, linking its absence to eNOS hyperactivity and dilated drainage vessels, but not outflow facility reduction, suggesting a specific role beyond conventional outflow resistance.

Li Guorong, Torrejon Karen Y, Unser Andrea M, Ahmed Feryan, Navarro Iris D, Baumgartner Rudolf A et al.

Trabodenoson lowers IOP in mice by increasing outflow facility via TM extracellular matrix remodeling, suggesting a novel glaucoma treatment mechanism.

Wen Joanne C, Reina-Torres Ester, Sherwood Joseph M, Challa Pratap, Liu Katy C, Li Guorong et al.

Chronic anti-VEGF injections reduce aqueous outflow facility, particularly with many injections and pre-existing ocular hypertension. Clinicians should monitor IOP in these patients for glaucoma risk.

Reina-Torres Ester, Wen Joanne C, Liu Katy C, Li Guorong, Sherwood Joseph M, Chang Jason Y H et al.

This study found VEGF, secreted by TM cells under stress, increases aqueous outflow facility via VEGFR-2, suggesting anti-VEGF therapies may reduce outflow and cause ocular hypertension.

Ren Ruiyi, Li Guorong, Le Thuy Duong, Kopczynski Casey, Stamer W Daniel, Gong Haiyan

Netarsudil-M1 significantly boosts outflow facility in human eyes by expanding juxtacanalicular tissue and dilating episcleral veins, redistributing aqueous flow. This explains its glaucoma-treating mechanism.

Li Guorong, Luna Coralia, Gonzalez Pedro

This study found miR-183 inhibits DNA repair and proliferation in human trabecular meshwork cells by targeting KIAA0101. This suggests miR-183 contributes to glaucoma-related cellular senescence.

Wu Jing, Li Guorong, Luna Coralia, Spasojevic Ivan, Epstein David L, Gonzalez Pedro

Trabecular meshwork cells produce extracellular adenosine, mainly via CD73, which is vital for regulating aqueous humor outflow. Disrupting this pathway decreases outflow, suggesting a glaucoma mechanism.

Luna Coralia, Li Guorong, Qiu Jianming, Epstein David L, Gonzalez Pedro

This study found TGFβ2 downregulates miR-29 in trabecular meshwork cells, increasing ECM. miR-29b also inhibits TGFβ1. This crosstalk is crucial for outflow pathway regulation and glaucoma pathogenesis.

Li Guorong, Luna Coralia, Qiu Jianming, Epstein David L, Gonzalez Pedro

MiR-204 in glaucoma's drainage cells (HTM) was studied, finding it increases cell death and oxidative damage while reducing inflammation and ER stress response. This suggests miR-204 critically influences HTM health, impacting glaucoma pathogenesis.

Li Guorong, Luna Coralia, Qiu Jianming, Epstein David L, Gonzalez Pedro

Studying senescent HTM cells, researchers found miR-146a upregulation reduced inflammation and improved cell function. This suggests miR-146a could protect the trabecular meshwork from age-related damage in glaucoma.

Luna Coralia, Li Guorong, Qiu Jianming, Challa Pratap, Epstein David L, Gonzalez Pedro

Studied how mechanical stress releases ATP in eye cells, finding it mobilizes arachidonic acid and protective PGE2. This suggests a mechanism for glaucoma and potential therapeutic targets.

Liton Paloma B, Lin Yizhi, Luna Coralia, Li Guorong, Gonzalez Pedro, Epstein David L

Chronic oxidative stress in TM cells impairs lysosomal function, leading to waste accumulation. This suggests oxidative stress contributes to age-related TM dysfunction and glaucoma.