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.
N1 - Funding Information:
This work was partly supported by an unrestricted grant to University of Miami from Research to Prevent Blindness, NIH grants EY016112 and EY14801, Department of Defense grant W81XWH-15-1-0079. Fig.?2 B?F and Fig.?9 A & B are courtesy of the Johnstone Glaucoma Laboratory at the University of Washington.
Publisher Copyright:
© 2016 The Authors
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 - Segmental outflow
KW - Trabecular meshwork
KW - schlemm's canal
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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 Research
JF - Progress in Retinal Research
SN - 1350-9462
ER -