The lens is an important determinant of overall vision quality whose refractive and transparent properties change throughout life. Alterations to the refractive properties of the lens contribute to the process of emmetropisation in early childhood, and then the gradual loss in lens power that occurs throughout adulthood. In parallel to these changes to lens refractive power, age-dependent increases in lens stiffness and light scattering result in presbyopia and cataract, respectively. In recent years it has been confirmed that the lens operates an internal microcirculation system that generates circulating fluxes of ions, water and nutrients that maintain the refractive properties and transparency of the lens. By actively regulating lens water content, the microcirculation system controls two key parameters, lens geometry and the gradient of refractive index, which together determine the refractive properties of the lens. Furthermore, by delivering nutrients and antioxidants to the lens nucleus, the microcirculation system maintains lens transparency by preventing crystallin aggregation. Interestingly, the solubility, intramolecular packing and refractive index increment of crystallin proteins can be modulated by the ability of crystallin proteins to dynamically bind water, a processed called syneresis. In a series of previous studies it has been shown that the application of external pressure to the lens can induce syneresis. Since it is now known that lens water transport generates a substantial internal hydrostatic pressure gradient, we speculate that the microcirculation is capable of regulating crystallin function by altering the amount of water bound to lens proteins in the nucleus, where the pressure gradient and protein concentrations are the highest. Here we present evidence for the links between lens transport, pressure, syneresis and protein function. Furthermore, because the lens pressure gradient can be regulated by intrinsic and extrinsic stimuli, we suggest mechanisms via which this integrative system can be used to effect the changes to the refractive and transparent properties of the lens that are observed across our lifetime.

晶状体是整体视觉质量的重要决定因素，其折射和透明特性在整个生命周期中都会发生变化。晶状体屈光特性的改变会导致儿童早期的正视化过程，然后导致整个成年期晶状体屈光力的逐渐丧失。与晶状体屈光力的这些变化并行，晶状体硬度和光散射随年龄的增加分别导致老花眼和白内障。近年来，已证实晶状体具有内部微循环系统，可产生离子、水和营养物质的循环通量，从而维持晶状体的折射特性和透明度。通过主动调节镜片含水量，微循环系统控制两个关键参数，镜片的几何形状和折射率的梯度共同决定了镜片的折射特性。此外，通过向晶状体核输送营养物质和抗氧化剂，微循环系统通过防止晶状体蛋白聚集来保持晶状体透明度。有趣的是，晶状体蛋白的溶解度、分子内堆积和折射率增量可以通过晶状体蛋白动态结合水的能力来调节，这一过程称为脱水收缩。之前的一系列研究表明，对晶状体施加外部压力会引起脱水收缩。由于现在已知晶状体水传输会产生显着的内部静水压力梯度，我们推测微循环能够通过改变细胞核中与晶状体蛋白结合的水量来调节晶状体蛋白功能，其中压力梯度和蛋白质浓度最高。在这里，我们提供了晶状体运输、压力、脱水收缩和蛋白质功能之间联系的证据。此外，由于晶状体压力梯度可以通过内在和外在刺激来调节，因此我们提出了一种机制，通过该机制，可以使用该集成系统来影响我们一生中观察到的晶状体的折射和透明特性的变化。