Severity of optic nerve damage in eyes with POAG is correlated with changes in the trabecular meshwork.

Gottanka, Johannes; Johnson, Douglas H.; Martus, Peter; Lütjen–Drecoll, Elke

doi:10.1016/s0002-9394(14)71681-2

Cited by 76 publications

(60 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…22 These changes appear to be closely related to the disease process, because there is a negative correlation between the sheath-derived plaque material and axon counts. 23 The mechanisms that trigger changes in the trabecular meshwork in glaucoma are not well described. A molecule that appears to play an important role in the trabecular meshwork changes in glaucoma is transforming growth factor-b2, which also may be involved in some of the glaucomatous processes at the posterior pole of the eye, including impairment of axonal transport and neurotrophic supply.…”

Section: Pathophysiology Of Glaucomamentioning

confidence: 99%

Pharmacotherapy of Glaucoma

Schmidl

Schmetterer²,

Garhöfer³

et al. 2015

Journal of Ocular Pharmacology and Therapeutics

136

View full text Add to dashboard Cite

Glaucoma is a group of diseases involving the optic nerve and associated structures, which is characterized by progressive visual field loss and typical changes of the optic nerve head (ONH). The only known treatment of the disease is reduction of intraocular pressure (IOP), which has been shown to reduce glaucoma progression in a variety of large-scale clinical trials. Nowadays, a relatively wide array of topical antiglaucoma drugs is available, including prostaglandin analogues, carbonic anhydrase inhibitors, beta-receptor antagonists, adrenergic agonists, and parasympathomimetics. In clinical routine, this allows for individualized treatment taking risk factors, efficacy, and safety into account. A major challenge is related to adherence to therapy. Sustained release devices may help minimize this problem but are not yet available for clinical routine use. Another hope arises from non-IOP-related treatment concepts. In recent years, much knowledge has been gained regarding the molecular mechanisms that underlie the disease process in glaucoma. This also strengthens the hope that glaucoma therapy beyond IOP lowering will become available. Implementing this concept with clinical trials remains, however, a challenge.

show abstract

Section: Pathophysiology Of Glaucomamentioning

confidence: 99%

Pharmacotherapy of Glaucoma

Schmidl

Schmetterer²,

Garhöfer³

et al. 2015

Journal of Ocular Pharmacology and Therapeutics

136

View full text Add to dashboard Cite

show abstract

“…The observed increase in extracellular matrix in the outer TM may contribute to the increase in outflow resistance as seen in normal elderly eyes [27]. Furthermore, in previous studies the amount of sheath derived (SD)-plaques have been shown to be significantly greater in glaucomatous compared to normal age-matched eyes [8,33] suggesting that the excess of this material found in POAG eyes may also be responsible for the elevation of IOP.…”

Section: Discussionmentioning

confidence: 93%

“…Increased resistance to aqueous humor outflow, leading to the elevation of IOP, is a dominant risk factor for glaucoma [25,[27][28][29]. The structures responsible for such an increase include JCT and SC [30][31][32][33]. In a recent paper Overby et al [11] showed that endothelium of the Schlemm's canal that lead to pore formation modulates the outflow resistance.…”

Section: Discussionmentioning

confidence: 99%

Elevated Intraocular Pressure induces Ultrastructural Changes in the Trabecular Meshwork

Vecino¹,

GaldósM²,

Bayón³

et al. 2015

J Cytol Histol

View full text Add to dashboard Cite

The elevation of intraocular pressure (IOP) can be caused by the obstruction of flow in the trabecular meshwork and the age of the individuals has been pointed as one risk factor influencing in developing glaucoma. This study was designed to elucidate the morphological and ultrastructural changes in the trabecular meshwork of young adult Göttingen minipigs eyes after experimentally inducing a moderated chronic elevation of intraocular pressure lasting for over 14 months. The method used was cauterization of episcleral veins, located post-trabecular in the flow pathway and thus not affecting the cells located in the trabecular meshwork. The tissue was analysed using electron microscopy in control and experimental eyes. An increase in the amount of fibrillar material in the subendothelial region with a decreased optically empty spaces and an increase in rough endoplasmic reticulum (rER) were observed in the young experimental eyes. By experimentally increasing the post-trabecular resistance to the aqueous outflow, the present study showed that IOP elevation led to ultrastructural changes and thus concluded that changes in the trabecular meshwork can take place not only due to the advanced age, but by mechanical action on the cells as well.

show abstract

“…Moreover, in vivo studies in humans have shown that both intraocular pressure increase and visual field damage are significantly related to the amount of oxidative DNA damage (Sacca et al, 2005). Similarly, severity of optic nerve damage in eyes with primary open-angle glaucoma is correlated with changes in the trabecular meshwork (Gottanka et al, 1997). MicroRNA (miRNA) are an abundant class of noncoding small (~22 nucleotides) RNAs that modulate gene expression at the post-transcriptional level and participate in the regulation of many cellular functions (Wu et al, 2006;Filipowicz et al, 2008;Stefani et al, 2008) Specifically, miR-29b has been demonstrated to regulate multiple genes coding for extracellular matrix proteins, including multiple collagens, fibrillins, and elastin (Luna et al, 2009b).…”

Section: Introductionmentioning

confidence: 99%