NLRP3 Inflammasome and Pathobiology in AMD

Journal of Clinical Medicine

Lucia Celkova¹  Sarah L. Doyle²  Matthew Campbell¹ 

[1] Neurovascular Genetics Laboratory, Smurfit Institute of Genetics, Trinity College Dublin, Lincoln Place Gate, Dublin 2, Ireland; E-Mail:;Department of Clinical Medicine, School of Medicine, Trinity College Dublin, Dublin 2, Ireland; E-Mail:

关键词: age-related macular degeneration;    NLRP3 inflammasome;    IL-18;    geographic atrophy;    choroidal neovascularization;    retinal pigment epithelium;    pyroptosis;    autophagy;   

DOI  :  10.3390/jcm4010172

来源: mdpi

【 摘 要 】

Age-related macular degeneration (AMD) is the leading cause of central vision loss and blindness in the elderly. It is characterized by a progressive loss of photoreceptors in the macula due to damage to the retinal pigment epithelium (RPE). Clinically, it is manifested by drusen deposition between the RPE and underlying choroid and accumulation of lipofuscin in the RPE. End-stage disease is characterized by geographic atrophy (dry AMD) or choroidal neovascularization (wet AMD). The NLRP3 inflammasome has recently been implicated in the disease pathology. Here we review the current knowledge on the involvement of this multiprotein complex and its effector cytokines interleukin-1β (IL-1β) and IL-18 in AMD progression. We also describe cell death mechanisms that have been proposed to underlie RPE degeneration in AMD and discuss the role of autophagy in the regulation of disease progression.

【 授权许可】

CC BY   
© 2015 by the authors; licensee MDPI, Basel, Switzerland.