scholarly journals Oxidative Stress Modulates Complement Factor H Expression in Retinal Pigmented Epithelial Cells by Acetylation of FOXO3

2007 ◽  
Vol 282 (31) ◽  
pp. 22414-22425 ◽  
Author(s):  
Zhihao Wu ◽  
Thomas W. Lauer ◽  
Anna Sick ◽  
Sean F. Hackett ◽  
Peter A. Campochiaro
Nature ◽  
2011 ◽  
Vol 478 (7367) ◽  
pp. 76-81 ◽  
Author(s):  
David Weismann ◽  
Karsten Hartvigsen ◽  
Nadine Lauer ◽  
Keiryn L. Bennett ◽  
Hendrik P. N. Scholl ◽  
...  

Biomedicines ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 763
Author(s):  
Sara Romero-Vazquez ◽  
Víctor Llorens ◽  
Alba Soler-Boronat ◽  
Marc Figueras-Roca ◽  
Alfredo Adan ◽  
...  

Age-related macular degeneration (AMD) heads the list of legal blindness among the elderly population in developed countries. Due to the complex nature of the retina and the variety of risk factors and mechanisms involved, the molecular pathways underlying AMD are not yet fully defined. Persistent low-grade inflammation and oxidative stress eventually lead to retinal pigment epithelium dysfunction and outer blood–retinal barrier (oBRB) breakdown. The identification of AMD susceptibility genes encoding complement factors, and the presence of inflammatory mediators in drusen, the hallmark deposits of AMD, supports the notion that immune-mediated processes are major drivers of AMD pathobiology. Complement factor H (FH), the main regulator of the alternative pathway of the complement system, may have a key contribution in the pathogenesis of AMD as it is able to regulate both inflammatory and oxidative stress responses in the oBRB. Indeed, genetic variants in the CFH gene account for the strongest genetic risk factors for AMD. In this review, we focus on the roles of inflammation and oxidative stress and their connection with FH and related proteins as regulators of both phenomena in the context of AMD.


2016 ◽  
Vol 240 (4) ◽  
pp. 495-506 ◽  
Author(s):  
Lei Wang ◽  
Marisol Cano ◽  
Sayantan Datta ◽  
Hong Wei ◽  
Katayoon B Ebrahimi ◽  
...  

2013 ◽  
Vol 51 (2) ◽  
pp. 59-66 ◽  
Author(s):  
Andreas W.A. Weinberger ◽  
Cordula Eddahabi ◽  
Dörthe Carstesen ◽  
Peter F. Zipfel ◽  
Peter Walter ◽  
...  

2020 ◽  
Author(s):  
Angela Armento ◽  
Sabina Honisch ◽  
Vasiliki Panagiotakopoulou ◽  
Inga Sonntag ◽  
Anke Jacob ◽  
...  

AbstractAge-related macular degeneration (AMD) is the leading cause of blindness in the elderly population. About 50% of AMD patients present polymorphisms in the Complement Factor H (CFH) gene, coding for Factor H protein (FH). AMD-associated CFH risk variants, Y402H in particular, impair FH function leading to complement overactivation. In AMD, retinal homeostasis is compromised due to dysfunction of retinal pigment epithelium (RPE) cells. Whether FH contributes to AMD pathogenesis only via complement system dysregulation remains unclear. To investigate the potential role of FH on energy metabolism and oxidative stress in RPE cells, we silenced CFH in human hTERT-RPE1 cells. FH-deprived RPE cells exposed to oxidative insult, showed altered metabolic homeostasis, including reduction of glycolysis and mitochondrial respiration, paralleled by an increase in lipid peroxidation. Our data suggest that FH protects RPE cells from oxidative stress and metabolic reprogramming, highlighting a novel function for FH in AMD pathogenesis.Graphical abstract


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