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3.4 IGFI与青光眼 研究表明，人眼小梁网组织与体外培养的人眼小梁网细胞均表达IGFI受体基因[35]。用放射配体结合实验研究证实，体外培养的猪眼小梁网细胞上也有高度亲和IGFI的受体基因[36]。Cao等[37]对体外培养牛小梁网组织研究表明小梁网细胞可产生IGFI，是房水和小梁网微环境中IGFI的来源，IGFI通过自分泌和旁分泌作用影响小梁网功能。IGFI对体外培养的人眼小梁网细胞增殖有明显的促进作用。Ando等[38]在体外培养猪小梁网细胞,研究表明包括IGFI的生长因子可引起眼压降低、小梁网细胞增殖和功能激活。因此，IGFI及其受体在维持小梁网正常功能可能起一定作用，其异常可能与POAG的发病有关。对小梁网IGFI表达的研究有助于探讨POAG的发病机制，为POAG的临床治疗提供新思路。
3.5 IGFI与近视 随着近视眼发病机制的研究不断深入，IGFI在近视发病中所起的作用也越来越受到重视，它通过与IGFIR结合，对眼轴生长和近视形成起重要作用。目前国内外多数学者已经通过体外培养细胞及实验性近视等途径发现IGFI可促进巩膜软骨细胞的增生，抑制纤维母细胞的增加和胞外基质的合成，促进巩膜的生长、增生等，从而提出IGFI与近视的发生发展有关。吕秀芳等[39]通过对近视儿童与正常儿童对照研究结果表明，近视组血清IGFI浓度较对照组明显升高，且与近视程度、眼轴长度呈正相关。邓志宏等[40]在鸡形觉剥夺性近视研究表明,随着实验眼近视屈光度增加、眼轴延长的同时，其后极部巩膜IGFIRmRNA的表达水平明显高于对照眼。Rada等[41]在实验性近视中发现剥夺性近视后巩膜组织中金属蛋白酶抑制因子减少，金属蛋白酶和金属蛋白酶抑制因子失衡，使得金属蛋白酶活性增强，导致近视的发生。因此有学者推测IGFI在近视中的机制为：IGFI作为一种近视信使，可能是通过影响血管内皮细胞释放降解胞外基质的金属蛋白酶，从而影响巩膜成纤维细胞生长以及胞外基质的合成，引起巩膜变薄、巩膜重新塑型、眼轴延长而出现近视。
3.6 IGFI与玻璃体疾病 高方等[42]用放射免疫测定法研究表明，由外伤、糖尿病、孔源性视网膜脱离等原因引起的增殖性玻璃体视网膜病变(PVR)，其玻璃体中IGFI含量明显高于正常对照组。苏颖等[43]测定外伤性玻璃体积血患者血清IGFI水平明显高于正常人。IGFI有促进细胞增殖并参与修复的功能。在血管受损时，它通过内皮细胞对损伤的反应促进细胞产生生长因子，经自分泌或旁分泌刺激自身和周围细胞生长与增殖。病理情况下这种平衡被打破。有研究表明，玻璃体内注射IGFI可能诱导血管扩张，微血管形成，以及新生血管的形成[44]。综上所述IGFI在这些增殖性病变的发生发展中可能起到重要作用。
随着对IGFI及其系统认识的深入，它们与眼外肌疾病、青光眼、白内障、近视、玻璃体及视网膜病变等相关疾病的关系将进一步阐明，有可能为上述眼病的预防和治疗提供一种新的思路与方法。
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