Abstract
Neovascular age-related macular degeneration (nAMD) is one of the leading causes of blindness among the aging population. The current treatment options for nAMD include intravitreal injections of anti-vascular endothelial growth factor (anti-VEGF). However, standardized frequent administration of anti-VEGF injections only improves vision in approximately 30–40% of nAMD patients. Current therapies targeting nAMD pose a significant risk of retinal fibrosis and geographic atrophy (GA) development in nAMD patients. A need exists to develop new therapies to treat nAMD with effective and long-term anti-angiogenic effects. Recent research on nAMD has identified novel therapeutic targets and angiogenic signaling mechanisms involved in its pathogenesis. For example, tissue factor, human intravenous immune globulin, interferon-β signaling, cyclooxygenase-2 (COX-2) and cytochrome P450 monooxygenase lipid metabolites have been identified as key players in the development of angiogenesis in AMD disease models. Furthermore, novel therapies such as NACHT, LRR and PYD domains containing protein 3 (NLRP3) inflammasome inhibition, inhibitors of integrins and tissue factor are currently being tested at the level of clinical trials to treat nAMD. The aim of this review is to discuss the scope for alternative therapies proposed as anti-VEGFs for the treatment of nAMD.
Highlights
Age related macular degeneration (AMD) is the most common cause of irreversible blindness among the elderly population [1,2]
This study discovered a novel mechanism involved in attenuating choroidal neo-vascularization (CNV) independent of vascular endothelial growth factor (VEGF) signaling, suggesting that recombinant IL-33 therapy could serve as an alternative treatment for Neovascular age-related macular degeneration (nAMD) patients who do not respond to conventional anti-VEGF treatments
Since the primary aim of this review is to focus on the pathways independent to VEGF, other signaling pathways that inhibit VEGF directly or indirectly with possible therapeutic benefits in nAMD are not discussed in detail, but are listed in form of table (Table 1), briefly discussing the involvement of key molecules, signaling pathways, and their mechanisms of action
Summary
Age related macular degeneration (AMD) is the most common cause of irreversible blindness among the elderly population [1,2]. AMD can be classified into early, intermediate, and advanced forms, depending on the severity of the symptoms [4,5]. The advanced form of AMD is known as geographic atrophy (GA) and is characterized by the loss of RPE and choroid near the macular region leading to the loss of photoreceptors and central vision [4,5]. The severe form of AMD (exudative) presents with growth of abnormal blood vessels from the choroid extending into the avascular RPE and sub-retinal regions. This phenomenon is known as choroidal neo-vascularization (CNV) and the form of AMD with CNV is termed nAMD [4,5]. This phenomenon is known as choroidal neo-vascularization (CNV) and the form of AMD with CNV is termed nAMD [4,5]. nAMD accounts for the majority of cases of blindness in AMD patients [1,3]
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