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3红细胞生成素与糖尿病视网膜病变
红细胞生成素（erythropoietin，EPO）由165个氨基酸组成的多功能蛋白质，在视网膜内主要表达在无长突细胞及双极细胞上，而其受体位于神经节细胞、无长突细胞及星形胶质细胞。EPO除有促造血、神经发生和神经保护（对抗缺血再灌注损伤和光诱导的视网膜退化）功能外，还能促进血管新生。在12～24wk早产儿玻璃体内EPO,EPOmRNA及蛋白质随着孕周增加而提高，这意味着EPO与视网膜血管发育有一定的关系[22]，在成人DR患眼玻璃体内EPO浓度比对照组高，并且高于血浆浓度[23]。Watanabe等认为这与ROP的血管损伤导致新生血管形成机制类似，均是由缺氧诱导产生，而不是由血视网膜屏障破坏导致的渗漏，进而促进视网膜血管新生，同时在低氧诱导的视网膜病变鼠模型中阻断EPO将抑制视网膜新生血管的形成及内皮细胞增生。
4转化生长因子与糖尿病视网膜病变
转化生长因子（transforming growth factorβ，TGFβ）为抗血管生成因子，玻璃体内的亚型是TGFβ2。在视网膜周细胞及内皮细胞共同培养时TGFβ由周细胞产生，随后抑制内皮细胞生长。因为DR发病时周细胞减少，故TGFβ也相应减少，从而导致了内皮细胞无限制增生，对新生血管发生起去抑制作用。也有研究认为TGF总量在DR时并未改变，只是其活化部分的比例降低，与非缺血性眼病相比，活化部分在PDR时下降了1/3。这一现象出现的原因可能是TGF的活化过程受蛋白酶如纤溶酶的调节，而在PDR组α2抗纤维蛋白酶（纤溶酶的不可逆抑制剂）水平显著提高。此外，研究报道病龄相对长的糖尿病鼠肾脏中TGF1水平升高，这种细胞因子可能参与VEGFR2的过度表达和刺激VEGF表达。
5成纤维细胞生长因子与糖尿病视网膜病变
许多细胞因子和生长因子包括基本成纤维细胞生长因子（basic fibroblast growth factor，bFGF）参与DR的发病。DR新生血管的形成的一个重要机制为内皮细胞凋亡受抑制，从而促进内皮细胞存活，这一机制可由远距离生长因子通过PI3k/Akt信号通路和上调凋亡抑制蛋白——生存素及Bcl2而实现，bFGF在这两方面均有作用，一方面，能上调生存素及Bcl2的表达，另一方面，可以激活蛋白激酶Akt，因而促进了DR新生血管形成，有一些抗新生血管形成的研究还涉及到bFGF糖化，因为其降低了bFGF与肝素结合的高亲和力及促有丝分裂活性[24]。此外，激素能抑制由bFGF诱导的脉络膜微血管内皮细胞迁移及管道形成等。
6结缔组织生长因子与糖尿病视网膜病变
结缔组织生长因子（connective tissue growth factor，CTGF）是VEGF诱导的促血管生成原因子和强效促纤维化因子。CTGF增加成纤维细胞增生和促血管细胞外基质产生。细胞外基质（ECM）表达增加使基底膜增厚，从而导致是视网膜血管渗透性增加和细胞迁移，加速DR发生发展。STZ诱导的糖尿病鼠增加了CTGFmRNA的表达及CTGF蛋白在视网膜节细胞层聚集，但这一过程能被ACE抑制剂逆转[25]。
7肝细胞生长因子与糖尿病视网膜病变
肝细胞生长因子（hepatocyte growth factor，HGF）为间质衍生的多效因子，是二硫化物连接的异二聚体分子，由69kDa的Kringle结构域α链及34kDa的β链组成。HGF受体是cmet原癌基因产物（跨膜酪氨酸激酶）。HGF能调节细胞的活性及生长，是一个强效的血管生成因子，刺激内皮细胞活性，促进内皮细胞在细胞外基质中的分散。同时，HGF也是内皮生长因子，其促进有丝分裂活性与bFGF，VEGF,IL1及IL6相比是最强的，即能刺激内皮细胞活性及生长，导致新生血管形成。Nishimura等认为HGF及VEGF在PDR患眼玻璃体内浓度较对照组增高，且在活动性视网膜病变眼内比静止性视网膜病变眼内浓度要高，而HGF及VEGF的增高无相关性。至于HGF的作用途径，Tacchini认为是通过CJNK和PI3激酶诱导HIF1的产生，而HIF1能感知下降的氧分压从而激活HIF1目标基因——VEGF及EPO，据前所述，此两种因子均是强烈的促血管生成因子。
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