Kong Lingjie, Han Xiaoyan, Qi Siyi, Li Duo, Zhang Jingyue, Zhang Linyu, Zhang Shujie, Jiang Qin, Yan Biao, Zhao Chen
Eye Institute and Department of Ophthalmology, Eye & ENT Hospital, Fudan University, Shanghai, China.
Key Laboratory of Myopia and Related Eye Diseases, NHC; Key Laboratory of Myopia and Related Eye Diseases, Chinese Academy of Medical Sciences, Shanghai, China.
Aging Cell. 2026 Feb;25(2):e70377. doi: 10.1111/acel.70377.
Neovascular age-related macular degeneration (nAMD) is a major cause of irreversible vision impairment in elderly populations, characterized by pathological angiogenesis beneath the macula. Although anti-VEGF therapies have demonstrated clinical effectiveness, significant challenges including drug resistance and the need for frequent intravitreal injections persist. As natural nanovesicles, exosomes derived from mesenchymal stem cell (MSC) can mediate intercellular communication, making them an attractive alternative for modulating cellular processes. This study explored the anti-angiogenic effects of MSC-derived exosomes in nAMD, with particular emphasis on the role of a specific exosomal lncRNA lnc-AGT-3. Our results showed that lnc-AGT-3 expression was reduced in both nAMD patients and choroidal neovascularization (CNV) models, and its overexpression effectively inhibited pathological angiogenesis in vitro and in vivo. Mechanistically, lnc-AGT-3 enhanced the p53 signaling pathway by blocking the ubiquitination and degradation of p53 and ultimately inhibited neovascularization, a process potentially linked to its direct interaction with heterogeneous nuclear ribonucleoprotein K (hnRNP K). Our findings position MSC-derived exosomes enriched with lnc-AGT-3 as an innovative therapeutic paradigm for nAMD, acting through p53 pathway modulation to potentially overcome current treatment limitations.
新生血管性年龄相关性黄斑变性(nAMD)是老年人群不可逆视力损害的主要原因,其特征是黄斑下的病理性血管生成。尽管抗VEGF疗法已显示出临床疗效,但包括耐药性和频繁玻璃体内注射的需求等重大挑战仍然存在。作为天然纳米囊泡,间充质干细胞(MSC)来源的外泌体可以介导细胞间通讯,使其成为调节细胞过程的有吸引力的替代方案。本研究探讨了MSC来源的外泌体在nAMD中的抗血管生成作用,特别强调了特定外泌体长链非编码RNA lnc-AGT-3的作用。我们的结果表明,lnc-AGT-3在nAMD患者和脉络膜新生血管(CNV)模型中的表达均降低,其过表达在体外和体内均有效抑制病理性血管生成。机制上,lnc-AGT-3通过阻断p53的泛素化和降解来增强p53信号通路,并最终抑制新生血管形成,这一过程可能与其与异质性核糖核蛋白K(hnRNP K)的直接相互作用有关。我们的研究结果将富含lnc-AGT-3的MSC来源的外泌体定位为nAMD的一种创新治疗模式,通过调节p53途径发挥作用,有可能克服当前的治疗局限性。