Abstract:
Age-related macular degeneration (AMD), a leading cause of irreversible blindness in adults, may result in poor central vision, making it difficult to see, read, and drive. AMD is generally classified in either dry or wet types. Milder cases of dry AMD may progress to geographic atrophy (GA), leading to significant visual disability; wet, or neovascular AMD, which involves choroidal neovascularization (CNV), can lead to complete loss of central vision. Adiponectin (APN) discovery in the mid-1990\'s and, subsequently, its two cognate receptors (AdipoRs) in the early 2000s have led to a remarkable progress in better understanding metabolic disorders, as well as metabolism-associated ocular pathology. APN/AdipoRs signaling plays a central role in a variety of molecular and cellular physiological events, including glucose and lipid metabolism, whole-body energy regulation, immune and inflammation responses, insulin sensitivity and retinal cell biological functions. This review is an amalgamation of recent information related to APN/AdipoRs in the pathophysiology of retinal diseases and furthers its association with AMD and diabetic retinopathy. Additionally, we present our original research, where we designed control peptide and CNV inhibitory peptide from the globular region of APN to see the effect of these peptides on the mouse model of laser-induced CNV. The inhibitory peptide (APN1) inhibited CNV by more than 75% while the control peptide did not inhibit CNV.
摘要:
年龄相关性黄斑变性(AMD),成人不可逆性失明的主要原因,可能会导致中央视力不佳,使它很难看到,阅读,和驱动器。AMD通常分为干型或湿型。干性AMD的轻度病例可能进展为地理萎缩(GA),导致严重视力障碍的;湿的,或新生血管性AMD,涉及脉络膜新生血管(CNV),会导致中央视力的完全丧失。脂联素(APN)在1990年代中期发现,随后,它的两个同源受体(AdipoRs)在2000年代初导致了在更好地理解代谢紊乱方面的显着进展,以及与代谢相关的眼部病理学。APN/AdipoRs信号在各种分子和细胞生理事件中起着核心作用,包括葡萄糖和脂质代谢,全身能量调节,免疫和炎症反应,胰岛素敏感性和视网膜细胞生物学功能。这篇综述是视网膜疾病病理生理学中与APN/AdipoRs相关的最新信息的融合,并进一步促进了其与AMD和糖尿病性视网膜病变的关系。此外,我们提出了我们的原始研究,我们从APN的球状区域设计了对照肽和CNV抑制肽,以观察这些肽对激光诱导的CNV小鼠模型的影响。抑制肽(APN1)抑制CNV超过75%,而对照肽不抑制CNV。