The Dynamics of Aqueous Humor Outflow—A Major Review

Ahmad, Syed Shoeb; Ghani, Shuaibah Abdul; Singh, Daljit; Wah, Lott Pooi

doi:10.17925/usor.2014.07.02.137

Cited by 4 publications

(2 citation statements)

References 32 publications

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“…The drainage of AH from the anterior segment at the iridocorneal angle occurs largely through TM and to a little extent via alternative uveoscleral pathway. 139…”

Section: Glaucomamentioning

confidence: 99%

“…The drainage of AH from the anterior segment at the iridocorneal angle occurs largely through TM and to a little extent via alternative uveoscleral pathway. 139 In the TM of POAG patients, excessive deposition of extracellular fibrillar material also known as "sheath-derived plaque material" has been detected. The plaque material consists of ECM elements such as elastic fibers, fibronectin, and collagen type IV.…”

Section: Glaucomamentioning

confidence: 99%

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Connective tissue growth factor: Role in trabecular meshwork remodeling and intraocular pressure lowering

Hassan,

Razali,

Abu Bakar

et al. 2023

Exp Biol Med (Maywood)

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Connective tissue growth factor (CTGF) is a distinct signaling molecule modulating many physiological and pathophysiological processes. This protein is upregulated in numerous fibrotic diseases that involve extracellular matrix (ECM) remodeling. It mediates the downstream effects of transforming growth factor beta (TGF-β) and is regulated via TGF-β SMAD-dependent and SMAD-independent signaling routes. Targeting CTGF instead of its upstream regulator TGF-β avoids the consequences of interfering with the pleotropic effects of TGF-β. Both CTGF and its upstream mediator, TGF-β, have been linked with the pathophysiology of glaucomatous optic neuropathy due to their involvement in the regulation of ECM homeostasis. The excessive expression of these growth factors is associated with glaucoma pathogenesis via elevation of the intraocular pressure (IOP), the most important risk factor for glaucoma. The raised in the IOP is due to dysregulation of ECM turnover resulting in excessive ECM deposition at the site of aqueous humor outflow. It is therefore believed that CTGF could be a potential therapeutic target in glaucoma therapy. This review highlights the CTGF biology and structure, its regulation and signaling, its association with the pathophysiology of glaucoma, and its potential role as a therapeutic target in glaucoma management.

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“…The drainage of AH from the anterior segment at the iridocorneal angle occurs largely through TM and to a little extent via alternative uveoscleral pathway. 139…”

Section: Glaucomamentioning

confidence: 99%

Section: Glaucomamentioning

confidence: 99%

Connective tissue growth factor: Role in trabecular meshwork remodeling and intraocular pressure lowering

Hassan,

Razali,

Abu Bakar

et al. 2023

Exp Biol Med (Maywood)

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A Review of Nitric Oxide for the Treatment of Glaucomatous Disease

2017

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Glaucoma is the leading cause of irreversible blindness worldwide, affecting 64.3 million people. An estimated 60.5 million people are affected by primary open angle glaucoma globally, and this will increase to 111.8 million by 2040. The definition of glaucoma has evolved greatly over time. Although multiple risk factors such as ischemia, inflammation, myopia, race, age and low ocular perfusion pressure may play a role, intraocular pressure (IOP) is still the main risk factor we can easily identify and modify. Currently, both medical and surgical interventions aim to reduce IOP. Effective IOP reduction controls and prevents the progression in many cases of glaucoma. Although this multifactorial disease’s true pathophysiology is difficult to elucidate, physiologic mediators including nitric oxide (NO) are being evaluated as novel ways to impact progression by both lowering IOP and improving optic nerve head perfusion. Latanoprostene bunod 0.024% is an emerging therapeutic agent that has shown promise in clinical trials. As a nitric oxide-donating prostaglandin F2-alpha receptor agonist, it has proven to effectively, and with good tolerability, reduce IOP in glaucoma and ocular hypertensive patients. Latanoprostene bunod capitalizes on NO’s ability to modulate the conventional aqueous humor outflow system, directly improving outflow through the trabecular meshwork, Schlemm’s canal and distal scleral vessels. Importantly, targeting the conventional outflow tissues with NO-donating drugs represents an opportunity to restore outflow function, which will most likely have a beneficial consequence of additional IOP-lowering effects with dampening of diurnal and other IOP fluctuations, the benefit of a healthy trabecular meshwork.

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Pharmacologic Trabeculectomy—Modulation of Aqueous Humor Outflow Through the Trabecular Meshwork

Ahmad¹,

Zia-ur-Rahman²,

Ramli³

et al. 2015

US Ophthalmic Review

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“Pharmacologic trabeculectomy” is a term used to describe the modulation of aqueous outflow by the biochemical manipulation of the trabecular meshwork. Most of the medications currently in use either reduce aqueous production or increase its outflow through the ciliary body. However, there is a new group of agents being investigated, which can increase the facility of aqueous humor outflow through the trabecular meshwork. Thus, these agents will be able to provide a more physiologic means to control aqueous humor dynamics. This review sheds light on this concept of “medical trabeculectomy.”

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The Dynamics of Aqueous Humor Outflow—A Major Review

Cited by 4 publications

References 32 publications

Connective tissue growth factor: Role in trabecular meshwork remodeling and intraocular pressure lowering

Connective tissue growth factor: Role in trabecular meshwork remodeling and intraocular pressure lowering

A Review of Nitric Oxide for the Treatment of Glaucomatous Disease

Pharmacologic Trabeculectomy—Modulation of Aqueous Humor Outflow Through the Trabecular Meshwork

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