美国爱荷华大学一项研究提出，一种降低眼内压力并且防止青光眼小鼠的神经元流失的细胞替换疗法可能有潜力保存病人的视力。青光眼是全世界不可逆视力减退与失明的最常见原因。视力减退是由视网膜神经节细胞因为眼内压力升高而死亡造成的，而眼内压是由小梁网状组织(TM)细胞调控的。Markus Kuehn及其同事发现，移植来源于干细胞的小梁网状组织(TM)细胞，能降低眼内压力并防止患青光眼的小鼠的视网膜神经节细胞的死亡。这组作者对来自小鼠的皮肤细胞进行了遗传重编程，把它们变成了诱导多能干细胞(iPSCs)，后者然后被转化成了小梁网状组织(TM)细胞。之后，这组作者把iPSC-TM细胞或者作为对照的同等体积的生理盐水注射到了小鼠的眼中，这些小鼠有一个遗传突变，该突变能导致人类青光眼。与注射生理盐水不同，这种细胞替换疗法在至少9周时间里防止了眼内压升高的发展，并且保存了小梁网状组织(TM)细胞和视网膜神经节细胞的数量。额外的证据提示，与移植的iPSC-TM细胞的直接接触可能刺激眼中已经存在的小梁网状组织(TM)细胞的增殖。这组作者提出，通过防止眼内压升高和神经元流失，细胞替换疗法可能有潜力保存青光眼病人的视力并增加生活质量。

原文摘要：Glaucoma is a common cause of vision loss or blindness and reduction of intraocular pressure (IOP) has been proven beneficial in a large fraction of glaucoma patients. The IOP is maintained by the trabecular meshwork (TM) and the elevation of IOP in open-angle glaucoma is associated with dysfunction and loss of the postmitotic cells residing within this tissue. To determine if IOP control can be maintained by replacing lost TM cells, we transplanted TM-like cells derived from induced pluripotent stem cells into the anterior chamber of a transgenic mouse model of glaucoma. Transplantation led to significantly reduced IOP and improved aqueous humor outflow facility, which was sustained for at least 9 wk. The ability to maintain normal IOP engendered survival of retinal ganglion cells, whose loss is ultimately the cause for reduced vision in glaucoma. In vivo and in vitro analyses demonstrated higher TM cellularity in treated mice compared with littermate controls and indicated that this increase is primarily because of a proliferative response of endogenous TM cells. Thus, our study provides in vivo demonstration that regeneration of the glaucomatous TM is possible and points toward novel approaches in the treatment of this disease.