Age-related macular degeneration (AMD) is a complex eye disease underlined by the death of photoreceptors and degeneration of retinal pigment epithelium (RPE) and choriocapillaris (CC). The mechanism(s) responsible for massive and progressive retinal degeneration is not completely known. Senescence, a state of permanent inhibition of cell growth, may be induced by many factors important for AMD pathogenesis and results in senescence-associated secretory phenotype (SASP) that releases growth factors, cytokines, chemokines, proteases and other molecules inducing inflammation and other AMD-related effects. These effects can be induced in the affected cell and neighboring cells, leading to progression of AMD phenotype. Senescent cells also release reactive oxygen species that increase SASP propagation. Many other pathways of senescence-related AMD pathogenesis, including autophagy, the cGAS-STING signaling, degeneration of CC by membrane attack complex, can be considered. A2E, a fluorophore present in lipofuscin, amyloid-beta peptide and humanin, a mitochondria-derived peptide, may link AMD with senescence. Further studies on senescence in AMD pathogenesis to check the possibility of opening a perspective of the use of drugs killing senescent cells (senolytics) and terminating SASP bystander effects (senostatics) might be beneficial for AMD that at present is an incurable disease.

中文翻译：

---

衰老在年龄相关性黄斑变性的发病机制中。


年龄相关性黄斑变性 (AMD) 是一种复杂的眼部疾病，其特点是光感受器死亡以及视网膜色素上皮 (RPE) 和脉络膜毛细血管 (CC) 变性。造成大规模进行性视网膜变性的机制尚不完全清楚。衰老是一种细胞生长永久抑制的状态，可能由许多对 AMD 发病机制重要的因素诱导，并导致衰老相关的分泌表型 (SASP)，释放生长因子、细胞因子、趋化因子、蛋白酶和其他诱导炎症和其他 AMD 的分子相关影响。这些效应可以在受影响的细胞和邻近细胞中诱导，导致 AMD 表型的进展。衰老细胞还会释放活性氧，从而增加 SASP 的增殖。衰老相关 AMD 发病机制的许多其他途径，包括自噬、cGAS-STING 信号传导、膜攻击复合物引起的 CC 退化，都可以考虑。 A2E 是存在于脂褐素、淀粉样β 肽和护脑素（一种线粒体衍生肽）中的荧光团，可能将 AMD 与衰老联系起来。对 AMD 发病机制中的衰老进行进一步研究，以检查是否有可能开启使用药物杀死衰老细胞（senolytics）和终止 SASP 旁观者效应（senostatics）的前景，这可能对目前无法治愈的 AMD 有益。