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.

在青光眼中，降低眼内压（IOP）可提供神经保护。眼压升高是青光眼的特征，由房水 (AH) 流出受损引起。小梁网 (TM) 是调节 AH 流出所必需的类似过滤器的结构，阻力增加可能会导致流出受损。通过 TM 结构 360° 圆周的流动可能是不均匀的，分为高流动区域和低流动区域，称为分段。流经 TM 后，AH 进入施累姆氏管 (SC)，该管表达血液和淋巴标记物；然后 AH 沿着 SC 外部井进入收集器通道入口 (CCE)。 AH 从 CCE 进入通常与 SC 平行的深部巩膜丛 (DSP)。从 DSP 开始，巩膜内收集血管径向延伸至巩膜表面，与含有 AH 的血管（称为房水静脉）连接，将 AH 排出至含有血液的巩膜外静脉。然而，维持内皮细胞沿通路稳态特性的分子机制尚不清楚。这些分子事件在衰老和青光眼病理学过程中如何变化仍未解决。在这篇综述中，我们提出了解释 AH 流出控制连续体的机制可能性，该连续体起源于 TM 并通过收集通道延伸到巩膜外静脉。