A systematic review of the literature was carried out by 2 independent reviewers using the PubMed and EMBASE electronic databases, searching for articles published in English from 2014/01/01 to 2019/07/01 using a combination of the following keywords: ("glaucoma" OR "ocular hypertension") AND ("electrophysiolog" OR "electroretinogra" OR "ERG" OR "mfERG" OR "Pattern-reversal electroretinography" OR "PERG" OR "mfPERG" OR "photopic negative response" OR "pattern electroretinogram" OR "visual evoked potential" OR "multifocal electroretinography" OR "multifocal electroretinogram" OR "electro-oculography" OR "multifocal VEP" OR "mf-ERG").
Although autotaxin, a secreted lysophospholipase D and its catalytic product lysophosphatidic acid (LPA) have been shown to modulate AH drainage through TM, we do not have a complete understanding of their role and regulation in glaucoma patients, TM and AH outflow.
Previous studies found that some pathways were related to glaucoma, such as extracellular matrix (ECM)-receptor interaction, phosphatidylinositol 3-kinase (PI3K)-protein kinase B (Akt) and apoptosis.
Since TRPC5 is a mechanosensor, it might function to sense abnormal intraocular pressure changes, and could contribute to the death of RGCs in diseases such as glaucoma.
CD9 is down-regulated in glaucoma, overexpression of CD9 can active integrin α4 (ITGA4), PI3K and Akt, which lead to the decreased apoptosis and attenuate glaucoma.
Further investigation is warranted of this newly proposed combination which may be particularly useful where access or experience with ECP or other minimally invasive glaucoma surgery is limited.
Although autotaxin, a secreted lysophospholipase D and its catalytic product lysophosphatidic acid (LPA) have been shown to modulate AH drainage through TM, we do not have a complete understanding of their role and regulation in glaucoma patients, TM and AH outflow.
The orphan G-protein-coupled receptor (GPCR) GPR158 is expressed in the brain, where it is involved in the osteocalcin effect on cognitive processes, and at the periphery, where it may contribute to glaucoma and cancers.
This study suggests that the automated structure-function report combining results from the SD-OCT and the HEP may assist in the evaluation and management of glaucoma.
<i>Conclusion:</i> In our experiments, glaucoma in FUS patients was associated with low levels of MCP-1 and MMP-9 in the AH, while expression of MMP-2, MMP-3, and TGFβ-1 increased.
Patients completed general health PROMs (European Quality of Life in 5 Dimensions [EQ-5D] and 36-item Short Form [SF-36]) and PROMs specific to glaucoma (15-item Glaucoma Quality of Life [GQL-15] and 9-item Glaucoma Activity Limitation [GAL-9]) at baseline and exit from the trial.
In conclusion, NR_003923 and IL22RA1 might contribute to glaucoma progression and be a novel and potential biomarkers and therapeutic targets for glaucoma.
Intracameral platelet-rich plasma (E-PRP) injection was an effective, rapidly effective, and safe procedure for treatment of severe chronic ocular hypotony following glaucoma filtrating surgery.
Inhibitor 2 was found to decrease ocular pressure by ∼4.5 mmHg in a sustained manner for at least 12 h after a single ocular application, underscoring the potential for topically-administered MGL inhibitors as a novel therapeutic target for the treatment of glaucoma.
Intracameral platelet-rich plasma (E-PRP) injection was an effective, rapidly effective, and safe procedure for treatment of severe chronic ocular hypotony following glaucoma filtrating surgery.
The orphan G-protein-coupled receptor (GPCR) GPR158 is expressed in the brain, where it is involved in the osteocalcin effect on cognitive processes, and at the periphery, where it may contribute to glaucoma and cancers.
We found significant differences in glucosylsphingosine lipids, consistent with decreased GBA and GBA2 and increased ASAH1 and ASAH2 immunoreactivity in glaucoma, suggesting the potential impairment of sphingolipid enzymatic pathways in lysosomal and nonlysosomal cellular compartments.
To date, various animal models of glaucoma have been established, including glutamate/aspartate transporter knockout (KO) mice, excitatory amino acid carrier 1 KO mice, optineurin E50K knock-in mice, DBA/2J mice and experimentally induced models.