青光眼是多因素退行性视神经病变疾病，其不可逆性与致盲性病理特点主要来自于该病对视神经的损伤，即青光眼性视神经病变(GON)。GON的治疗难点在于早期干预困难，且目前临床没有针对治疗所有类型GON的视神经保护药物。视网膜神经节细胞(RGCs)死亡是GON各种病因机制导致的核心病理改变，最新研究发现广泛分布的第二信使环腺苷3'，5'-单磷酸(cAMP)及其下游效应子蛋白激酶A(PKA)的信号级联传导在GON多种发病机制中产生重要影响，并可抑制RGCs凋亡，发挥对青光眼的视神经保护与治疗作用。因此文章对cAMP/PKA通路在GON病理生理发展过程中发挥的作用进行综述，重点关注其在青光眼眼压调节、氧化应激、神经炎症、视神经变性等方面的影响，以期为GON不同病理机制导致的视神经损伤寻找共通中枢调节靶点，推动对该病的进一步认识与临床治疗。

Glaucoma is a multifactorial degenerative optic neuropathy, and its irreversible and blinding pathological characteristics mainly come from the damage to the optic nerve, namely glaucomatous optic neuropathy(GON). The difficulty in the treatment of GON lies in the early intervention, and currently there is no optic neuroprotective drug for the treatment of all types of GON. The death of retinal ganglion cells(RGCs)is the core pathological change caused by various pathogenic mechanisms of GON. Recent studies have found that the widespread second messenger cyclic adenosine 3', 5' -monophosphate(cAMP)and its downstream effector protein kinase A(PKA)signal cascade play an important role in the pathogenesis of GON. It can also inhibit the apoptosis of RGCs and play a protective and therapeutic role in glaucoma. Therefore, this article reviews the role of cAMP/PKA pathway in the pathophysiological development of GON, focusing on its effects on glaucoma intraocular pressure regulation, oxidative stress, neuroinflammation and optic nerve degeneration, in order to find a common central regulatory target for the optic nerve damage caused by different pathological mechanisms of GON and promote the further understanding and clinical treatment of this disease.

国家自然科学基金资助项目(No.82274588); 国家中医药管理局人才支持项目[国中医药人教函(2022)6号]; 湖南省教育厅科研创新项目(No.CX20230790)