Complement activation and inflammatory processes in Drusen formation and age related macular degeneration.
By L. V. Johnson, William P. Leitner, Michelle K. Staples, Don H. Anderson. Experimental Eye Research, 2001
650 citations recorded by the source corpus.
Subfields: Ophthalmology, Radiology, Nuclear Medicine and Imaging
View Paper: https://www.semanticscholar.org/paper/134414c0cb675d4801946be2d57e441df089abb6
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In Ophthalmology
In Radiology, Nuclear Medicine and Imaging
Citations in the corpus
- The Pivotal Role of the Complement System in Aging and Age-related Macular Degeneration: Hypothesis Re-visited (2009, positive): “In the eye, MCP has been localized to RPE cells overlying drusen (Johnson et al., 2001) and, more recently, to the basolateral surface of RPE cells in situ (Fig.”
- The Impact of Oxidative Stress and Inflammation on RPE Degeneration in Non-neovascular AMD (2017, background): “We found that in intermediate disease, basal CD46 labeling was lost in areas overlying large drusen along with the immunolabeling of extracellular vesicular elements within drusen (Ebrahimi et al., 2012) (Fig 3), observations that were made also by Johnson et al (Johnson et al., 2001).”
- Age‐related macular degeneration—emerging pathogenetic and therapeutic concepts (2006, background): “Other drusen components including vitronectin (160), clusterin, complement receptor 1 (CR1), and membrane cofactor protein (MCP-1) (163) are known complement regulatory proteins.”
- Understanding age-related macular degeneration (AMD): Relationships between the photoreceptor/retinal pigment epithelium/Bruch’s membrane/choriocapillaris complex (2012, background): “capillary pillars of the choroid (Crabb et al., 2002; Johnson et al., 2001; Johnson et al., 2000) and in the vitreous of human eyes.”
- Current concepts in the pathogenesis of age-related macular degeneration. (2004, background): “The RPE cells respond to control dendritic cell activation by secreting proteins that modulate the immune response, including vitronectin, apolipoprotein E, and membrane cofactor protein.(137) Johnson and coworkers(137,147) pointed out that the cytoplasmic accumulation of vitronectin, apolipoprotein”
- Endoplasmic reticulum stress: molecular mechanism and therapeutic targets (2023, background): “As the lesion is aggravated, lipid-rich debris is laid down between the basal lamina of the RPE and the inner collagenous layer of Bruch’s membrane, involving RPE debris, lipids, minerals, and immune system-associated elements.(264) Risk factors for AMD involve both genetic and environmental factors”