Kaufman Paul L

Kaufman Paul L, Lütjen Drecoll Elke, Croft Mary Ann

Tan Junkai, Fan Ning, Wang Ningli, Feng BingKai, Yang Ming, Liu Guo et al.

Lentivirus-mediated C3 expression in trabecular meshwork cells significantly lowered rat intraocular pressure for over 40 days without inflammation, suggesting C3 gene therapy is a promising glaucoma treatment.

Kaufman Paul L, Mohr Mary E, Riccomini Scott P, Rasmussen Carol A

New glaucoma drugs targeting outflow, offering sustained delivery, and using novel mechanisms (gene/stem cell therapy) are emerging. These aim to improve patient adherence and outcomes by offering more tailored and effective long-term IOP control.

Michalik Aleksandra Z, Kaufman Paul L

Exfoliation glaucoma treatment often needs early polytherapy. New outflow-enhancing drugs targeting the trabecular meshwork may offer more effective, tailored management and potentially alter disease progression.

Weinreb Robert N, Liebmann Jeffrey M, Martin Keith R, Kaufman Paul L, Vittitow Jason L

Latanoprostene bunod (LBN) was studied for glaucoma/ocular hypertension. It significantly lowered intraocular pressure more effectively than timolol, offering a superior, well-tolerated treatment option for patients.

Aktas Zeynep, Rao Hongyu, Slauson Sarah R, Gabelt B'Ann T, Larsen Inna V, Sheridan Rachael T C et al.

Proteasome inhibition enhanced lentiviral gene delivery to trabecular meshwork cells and tissues. This could improve gene therapy for glaucoma by boosting therapeutic gene expression.

Siegfried Carla J, Shui Ying-Bo, Tian Baohe, Nork T Michael, Heatley Gregg A, Kaufman Paul L

Vitrectomy and lens extraction in macaques increased ocular oxygen, oxidative stress, and IOP. This suggests a link between increased oxygen exposure, oxidative damage, and open-angle glaucoma development.

Kaufman Paul L

Lu Wennan, Hu HuiLing, Sévigny Jean, Gabelt B'Ann T, Kaufman Paul L, Johnson Elaine C et al.

Chronic glaucoma models show sustained high extracellular ATP and altered purinergic signaling in the posterior eye. This suggests ATP plays a chronic role in glaucoma damage, offering new therapeutic targets.

Slauson Sarah R, Peters Donna M, Schwinn Marie K, Kaufman Paul L, Gabelt B'Ann T, Brandt Curtis R

Viral vectors enhance C3 transferase's ability to disrupt actin in eye cells and improve fluid outflow, suggesting a potential strategy for gene therapy delivery to treat glaucoma.

Weinreb Robert N, Ong Tuyen, Scassellati Sforzolini Baldo, Vittitow Jason L, Singh Kuldev, Kaufman Paul L

Latanoprostene bunod (LBN) 0.024% was studied against latanoprost for glaucoma. LBN 0.024% significantly lowered IOP more than latanoprost, offering a more effective treatment option.

Heyne Galen W, Kiland Julie A, Kaufman Paul L, Gabelt B'Ann T

Topical nitric oxide donor (SNP) significantly lowered monkey IOP by increasing outflow facility, suggesting NO-enhancing therapies could be useful for glaucoma.

Kaufman Paul L, Rasmussen Carol A

Gabelt B'ann T, Rasmussen Carol A, Tektas Ozan Y, Kim Charlene B Y, Peterson John C, Nork T Michael et al.

GDx VCC effectively detected early structural changes in experimental glaucoma, correlating with axon loss. Memantine showed potential neuroprotective effects, preserving visual function despite similar IOP exposure.

Weinreb Robert N, Kaufman Paul L

Lee Eun Suk, Gabelt B'ann T, Faralli Jennifer A, Peters Donna M, Brandt Curtis R, Kaufman Paul L et al.

Cochlin gene expression in monkey eye segments significantly decreased fluid outflow and increased pressure, suggesting its role in glaucoma and potential for creating glaucoma models.

Filla Mark S, Schwinn Marie K, Sheibani Nader, Kaufman Paul L, Peters Donna M

This study found distinct beta1 and beta3 integrin pathways converge to enhance CLAN formation in HTM cells, with different molecular dependencies. This suggests potential targets to reduce outflow resistance in glaucoma.

Buie LaKisha K, Rasmussen Carol A, Porterfield Eric C, Ramgolam Vinod S, Choi Vivian W, Markovic-Plese Silva et al.

Self-complementary AAV safely delivered genes to the trabecular meshwork in rats and monkeys, providing long-term expression without adverse effects. This supports gene therapy development for glaucoma.

Liu Xuyang, Rasmussen Carol A, Gabelt B'ann T, Brandt Curtis R, Kaufman Paul L

Gene therapy for glaucoma is advancing, with improved targeting and delivery bringing long-lasting, compliance-free treatment closer to reality for this chronic eye disease.

Weinreb Robert N, Kaufman Paul L

Bhattacharya Sanjoy K, Gabelt B'Ann T, Ruiz Jose, Picciani Renata, Kaufman Paul L

TGF-beta2 treatment in eye models increased intraocular pressure and cochlin levels. This suggests cochlin may be involved in glaucoma, but its exact role needs further study.

Toris Carol B, Gabelt B'Ann T, Kaufman Paul L

This review confirms topical prostaglandins primarily lower IOP by increasing uveoscleral outflow, with some trabecular outflow and flow stimulation, through extracellular matrix remodeling, crucial for glaucoma treatment.

Gonzalez Jose M, Hu Yujie, Gabelt B'Ann T, Kaufman Paul L, Peters Donna M

This study found the PPRARI sequence in fibronectin's Heparin II domain increases glaucoma outflow facility and disrupts trabecular meshwork cell actin, identifying a key target for therapy.

Schmidt Jimena F, Agapova Olga A, Yang Ping, Kaufman Paul L, Hernandez M Rosario

EphrinB1/EphB1 expression was studied in glaucoma models. Increased levels in early/moderate glaucoma suggest a protective role in limiting axonal damage and inflammation, potentially explaining macrophage activation in advanced disease.

Filla Mark S, Woods Anne, Kaufman Paul L, Peters Donna M

This study found beta1 and beta3 integrins cooperatively induce syndecan-4-containing cross-linked actin networks in human trabecular meshwork cells. This suggests integrin signaling could regulate outflow facility in glaucoma.