Research progress of cAMP/PKA signaling pathway in glaucoma optic neuropathy
10.3980/j.issn.1672-5123.2025.10.09
- VernacularTitle:cAMP/PKA信号通路在青光眼性视神经病变中的研究进展
- Author:
Hongda CUI
1
,
2
;
Yu HUANG
1
,
2
;
Xin XIA
1
,
2
;
Jiangwei LI
1
,
2
;
Qinghua PENG
1
,
2
Author Information
1. Hunan University of Chinese Medicine, Changsha 410208, Hunan Province, China
2. Department of Ophthalmology, the First Hospital of Hunan University of Chinese Medicine, Changsha 410007, Hunan Province, China
- Publication Type:Journal Article
- Keywords:
cyclic adenosine 3';
5' -monophosphate(cAMP);
protein kinase A(PKA);
glaucoma;
glaucomatous optic neuropathy;
retinal ganglion cells;
apoptosis
- From:
International Eye Science
2025;25(10):1598-1603
- CountryChina
- Language:Chinese
-
Abstract:
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.
