Circadian rhythm of intraocular pressure

Keisuke Ikegami
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Abstract

Intraocular pressure (IOP) plays a crucial role in glaucoma development, involving the dynamics of aqueous humor (AH). AH flows in from the ciliary body and exits through the trabecular meshwork (TM). IOP follows a circadian rhythm synchronized with the suprachiasmatic nucleus (SCN), the circadian pacemaker. The SCN resets peripheral clocks through sympathetic nerves or adrenal glucocorticoids (GCs). IOP's circadian rhythm is governed by circadian time signals, sympathetic noradrenaline (NE), and GCs, rather than the local clock. The activity of Na+/K+-ATPase in non-pigmented epithelial cells in the ciliary body can influence the nocturnal increase in IOP by enhancing AH inflow. Conversely, NE, not GCs, can regulate the IOP rhythm by suppressing TM macrophage phagocytosis and AH outflow. The activation of the β1-adrenergic receptor (AR)-mediated EPAC-SHIP1 signal through the ablation of phosphatidylinositol triphosphate may govern phagocytic cup formation. These findings could offer insights for better glaucoma management, such as chronotherapy.
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眼压的昼夜节律
眼内压(IOP)在青光眼的发展过程中起着至关重要的作用,涉及到房水(AH)的动态变化。房水从睫状体流入,通过小梁网(TM)流出。眼压的昼夜节律与昼夜节律起搏器上核(SCN)同步。SCN 通过交感神经或肾上腺糖皮质激素(GCs)重置外周时钟。眼压的昼夜节律受昼夜节律时间信号、交感神经去甲肾上腺素(NE)和糖皮质激素(GCs)的控制,而不是受本地时钟的控制。睫状体非色素上皮细胞中 Na+/K+-ATP 酶的活性可通过增强 AH 流入来影响眼压的夜间升高。相反,NE(而非 GCs)可通过抑制 TM 巨噬细胞的吞噬作用和 AH 流出来调节眼压节律。通过消减三磷酸肌醇,激活β1-肾上腺素能受体(AR)介导的EPAC-SHIP1信号可能会控制吞噬杯的形成。这些发现可为更好的青光眼治疗(如慢性疗法)提供启示。
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