Pk Lakshmi, Pawar Rajesh Singh, Katare Yogesh Kumar, Sudheesh M S
Dept. of Pharmacognosy, Amrita School of Pharmacy, AIMS Health Sciences Campus, Amrita Vishwa Vidyapeetham, Ponekkara, Kochi - 682041, India.
Faculty of Pharmacy, Jagran Lakecity University, Bhopal 462044, India.
ACS Pharmacol Transl Sci. 2025 Mar 26;8(4):932-950. doi: 10.1021/acsptsci.4c00583. eCollection 2025 Apr 11.
Diseases of multifactorial origin like neurodegenerative and autoimmune diseases require a multitargeted approach. The discovery of the role of autoimmunity in glaucoma and retinal ganglionic cell (RGC) death has led to a paradigm shift in our understanding of the etiopathology of glaucoma. Glaucoma can cause irreversible vision loss that affects up to an estimated 3% of the population over 40 years of age. The current pharmacotherapy primarily aims to manage only intraocular pressure (IOP), a modifiable risk factor in the glaucomatous neurodegeneration of RGCs. However, neurodegeneration continues to happen in normotensive patients (where the IOP is below a reference value), and the silent nature of the disease can cause significant visual impairment and take a massive toll on the healthcare system. Cannabinoids, although known to reduce IOP since the 1970s, have received renewed interest due to their neuroprotective, anti-inflammatory, and immunosuppressive effects on autoimmunity. Additionally, the role of the gut-retina axis and abnormal Wnt signaling in glaucoma makes cannabinoids even more relevant because of their action on multiple targets, all converging in the pathogenesis of glaucomatous neurodegeneration. Cannabinoids also cause epigenetic changes in immune cells associated with autoimmunity. In this Review, we are proposing the use of cannabinoids as a multitargeted approach for treating autoimmunity associated with glaucomatous neurodegeneration, especially for the silent nature of glaucomatous neurodegeneration in normotensive patients.
像神经退行性疾病和自身免疫性疾病这种多因素起源的疾病需要多靶点治疗方法。自身免疫在青光眼和视网膜神经节细胞(RGC)死亡中的作用的发现,导致了我们对青光眼病因病理学理解的范式转变。青光眼可导致不可逆的视力丧失,估计影响高达3%的40岁以上人群。目前的药物治疗主要旨在控制眼内压(IOP),这是RGC青光眼性神经变性中一个可改变的风险因素。然而,在眼压正常的患者(眼压低于参考值)中神经变性仍在继续,而且该疾病的隐匿性可导致严重的视力损害,并给医疗系统带来巨大负担。大麻素虽然自20世纪70年代就已知可降低眼压,但由于其对自身免疫的神经保护、抗炎和免疫抑制作用而重新受到关注。此外,肠-视网膜轴和异常Wnt信号在青光眼中的作用使大麻素更加相关,因为它们作用于多个靶点,所有这些靶点都汇聚在青光眼性神经变性的发病机制中。大麻素还会引起与自身免疫相关的免疫细胞的表观遗传变化。在本综述中,我们提议使用大麻素作为一种多靶点方法来治疗与青光眼性神经变性相关的自身免疫,特别是针对眼压正常患者中青光眼性神经变性的隐匿性。