Aqueous outflow - A continuum from trabecular meshwork to episcleral veins

Teresia Carreon, Elizabeth van der Merwe, Ronald L. Fellman, Murray Johnstone, Sanjoy K Bhattacharya

Research output: Contribution to journalReview article

30 Citations (Scopus)

Abstract

In glaucoma, lowered intraocular pressure (IOP) confers neuroprotection. Elevated IOP characterizes glaucoma and arises from impaired aqueous humor (AH) outflow. Increased resistance in the trabecular meshwork (TM), a filter-like structure essential to regulate AH outflow, may result in the impaired outflow. Flow through the 360° circumference of TM structures may be non-uniform, divided into high and low flow regions, termed as segmental. After flowing through the TM, AH enters Schlemm's canal (SC), which expresses both blood and lymphatic markers; AH then passes into collector channel entrances (CCE) along the SC external well. From the CCE, AH enters a deep scleral plexus (DSP) of vessels that typically run parallel to SC. From the DSP, intrascleral collector vessels run radially to the scleral surface to connect with AH containing vessels called aqueous veins to discharge AH to blood-containing episcleral veins. However, the molecular mechanisms that maintain homeostatic properties of endothelial cells along the pathways are not well understood. How these molecular events change during aging and in glaucoma pathology remain unresolved. In this review, we propose mechanistic possibilities to explain the continuum of AH outflow control, which originates at the TM and extends through collector channels to the episcleral veins.

Original languageEnglish (US)
Pages (from-to)108-133
Number of pages26
JournalProgress in Retinal and Eye Research
Volume57
DOIs
StatePublished - Mar 1 2017

Fingerprint

Trabecular Meshwork
Aqueous Humor
Veins
Glaucoma
Intraocular Pressure
Endothelial Cells
Pathology

Keywords

  • Basement membrane: turnover and stability
  • Collector channels
  • Continuum hypothesis
  • Deep scleral plexus
  • Distal outflow
  • Glaucoma
  • Mechanosensing
  • schlemm's canal
  • Segmental outflow
  • Trabecular meshwork

ASJC Scopus subject areas

  • Ophthalmology
  • Sensory Systems

Cite this

Aqueous outflow - A continuum from trabecular meshwork to episcleral veins. / Carreon, Teresia; van der Merwe, Elizabeth; Fellman, Ronald L.; Johnstone, Murray; Bhattacharya, Sanjoy K.

In: Progress in Retinal and Eye Research, Vol. 57, 01.03.2017, p. 108-133.

Research output: Contribution to journalReview article

Carreon, Teresia ; van der Merwe, Elizabeth ; Fellman, Ronald L. ; Johnstone, Murray ; Bhattacharya, Sanjoy K. / Aqueous outflow - A continuum from trabecular meshwork to episcleral veins. In: Progress in Retinal and Eye Research. 2017 ; Vol. 57. pp. 108-133.
@article{6642ed422cab4fbfa538d9cf11343f99,
title = "Aqueous outflow - A continuum from trabecular meshwork to episcleral veins",
abstract = "In glaucoma, lowered intraocular pressure (IOP) confers neuroprotection. Elevated IOP characterizes glaucoma and arises from impaired aqueous humor (AH) outflow. Increased resistance in the trabecular meshwork (TM), a filter-like structure essential to regulate AH outflow, may result in the impaired outflow. Flow through the 360° circumference of TM structures may be non-uniform, divided into high and low flow regions, termed as segmental. After flowing through the TM, AH enters Schlemm's canal (SC), which expresses both blood and lymphatic markers; AH then passes into collector channel entrances (CCE) along the SC external well. From the CCE, AH enters a deep scleral plexus (DSP) of vessels that typically run parallel to SC. From the DSP, intrascleral collector vessels run radially to the scleral surface to connect with AH containing vessels called aqueous veins to discharge AH to blood-containing episcleral veins. However, the molecular mechanisms that maintain homeostatic properties of endothelial cells along the pathways are not well understood. How these molecular events change during aging and in glaucoma pathology remain unresolved. In this review, we propose mechanistic possibilities to explain the continuum of AH outflow control, which originates at the TM and extends through collector channels to the episcleral veins.",
keywords = "Basement membrane: turnover and stability, Collector channels, Continuum hypothesis, Deep scleral plexus, Distal outflow, Glaucoma, Mechanosensing, schlemm's canal, Segmental outflow, Trabecular meshwork",
author = "Teresia Carreon and {van der Merwe}, Elizabeth and Fellman, {Ronald L.} and Murray Johnstone and Bhattacharya, {Sanjoy K}",
year = "2017",
month = "3",
day = "1",
doi = "10.1016/j.preteyeres.2016.12.004",
language = "English (US)",
volume = "57",
pages = "108--133",
journal = "Progress in Retinal and Eye Research",
issn = "1350-9462",
publisher = "Elsevier Limited",

}

TY - JOUR

T1 - Aqueous outflow - A continuum from trabecular meshwork to episcleral veins

AU - Carreon, Teresia

AU - van der Merwe, Elizabeth

AU - Fellman, Ronald L.

AU - Johnstone, Murray

AU - Bhattacharya, Sanjoy K

PY - 2017/3/1

Y1 - 2017/3/1

N2 - In glaucoma, lowered intraocular pressure (IOP) confers neuroprotection. Elevated IOP characterizes glaucoma and arises from impaired aqueous humor (AH) outflow. Increased resistance in the trabecular meshwork (TM), a filter-like structure essential to regulate AH outflow, may result in the impaired outflow. Flow through the 360° circumference of TM structures may be non-uniform, divided into high and low flow regions, termed as segmental. After flowing through the TM, AH enters Schlemm's canal (SC), which expresses both blood and lymphatic markers; AH then passes into collector channel entrances (CCE) along the SC external well. From the CCE, AH enters a deep scleral plexus (DSP) of vessels that typically run parallel to SC. From the DSP, intrascleral collector vessels run radially to the scleral surface to connect with AH containing vessels called aqueous veins to discharge AH to blood-containing episcleral veins. However, the molecular mechanisms that maintain homeostatic properties of endothelial cells along the pathways are not well understood. How these molecular events change during aging and in glaucoma pathology remain unresolved. In this review, we propose mechanistic possibilities to explain the continuum of AH outflow control, which originates at the TM and extends through collector channels to the episcleral veins.

AB - In glaucoma, lowered intraocular pressure (IOP) confers neuroprotection. Elevated IOP characterizes glaucoma and arises from impaired aqueous humor (AH) outflow. Increased resistance in the trabecular meshwork (TM), a filter-like structure essential to regulate AH outflow, may result in the impaired outflow. Flow through the 360° circumference of TM structures may be non-uniform, divided into high and low flow regions, termed as segmental. After flowing through the TM, AH enters Schlemm's canal (SC), which expresses both blood and lymphatic markers; AH then passes into collector channel entrances (CCE) along the SC external well. From the CCE, AH enters a deep scleral plexus (DSP) of vessels that typically run parallel to SC. From the DSP, intrascleral collector vessels run radially to the scleral surface to connect with AH containing vessels called aqueous veins to discharge AH to blood-containing episcleral veins. However, the molecular mechanisms that maintain homeostatic properties of endothelial cells along the pathways are not well understood. How these molecular events change during aging and in glaucoma pathology remain unresolved. In this review, we propose mechanistic possibilities to explain the continuum of AH outflow control, which originates at the TM and extends through collector channels to the episcleral veins.

KW - Basement membrane: turnover and stability

KW - Collector channels

KW - Continuum hypothesis

KW - Deep scleral plexus

KW - Distal outflow

KW - Glaucoma

KW - Mechanosensing

KW - schlemm's canal

KW - Segmental outflow

KW - Trabecular meshwork

UR - http://www.scopus.com/inward/record.url?scp=85009415019&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85009415019&partnerID=8YFLogxK

U2 - 10.1016/j.preteyeres.2016.12.004

DO - 10.1016/j.preteyeres.2016.12.004

M3 - Review article

C2 - 28028002

AN - SCOPUS:85009415019

VL - 57

SP - 108

EP - 133

JO - Progress in Retinal and Eye Research

JF - Progress in Retinal and Eye Research

SN - 1350-9462

ER -