Retinal ganglion cells, the neurons that die in glaucoma, are endowed with a high metabolism requiring optimal provision of oxygen and nutrients to sustain their activity. The timely regulation of blood flow is, therefore, essential to supply firing neurons in active areas with the oxygen and glucose they need for energy. Many glaucoma patients suffer from vascular deficits including reduced blood flow, impaired autoregulation, neurovascular coupling dysfunction, and blood-retina/brain-barrier breakdown. These processes are tightly regulated by a community of cells known as the neurovascular unit comprising neurons, endothelial cells, pericytes, Müller cells, astrocytes, and microglia. In this review, the neurovascular unit takes center stage as we examine the ability of its members to regulate neurovascular interactions and how their function might be altered during glaucomatous stress. Pericytes receive special attention based on recent data demonstrating their key role in the regulation of neurovascular coupling in physiological and pathological conditions. Of particular interest is the discovery and characterization of tunneling nanotubes, thin actin-based conduits that connect distal pericytes, which play essential roles in the complex spatial and temporal distribution of blood within the retinal capillary network. We discuss cellular and molecular mechanisms of neurovascular interactions and their pathophysiological implications, while highlighting opportunities to develop strategies for vascular protection and regeneration to improve functional outcomes in glaucoma.

视网膜神经节细胞是在青光眼中死亡的神经元，具有较高的新陈代谢能力，需要最佳的氧气和营养物质的供应来维持其活动。因此，及时调节血流对于为活跃区域的放电神经元提供能量所需的氧气和葡萄糖至关重要。许多青光眼患者患有血管缺陷，包括血流量减少、自动调节受损、神经血管耦合功能障碍和血视网膜/脑屏障破坏。这些过程受到称为神经血管单元的细胞群的严格调节，其中包括神经元、内皮细胞、周细胞、穆勒细胞、星形胶质细胞和小胶质细胞。在这篇综述中，神经血管单元占据了中心舞台，我们检查了其成员调节神经血管相互作用的能力以及它们的功能在青光眼应激期间如何改变。最近的数据表明，周细胞在生理和病理条件下神经血管耦合调节中发挥着关键作用，因此受到特别关注。特别令人感兴趣的是隧道纳米管的发现和表征，纳米管是连接远端周细胞的基于肌动蛋白的细导管，其在视网膜毛细血管网络内血液的复杂空间和时间分布中发挥着重要作用。我们讨论神经血管相互作用的细胞和分子机制及其病理生理学意义，同时强调制定血管保护和再生策略以改善青光眼功能结果的机会。