Choroidal neovascularization is the leading causes of central vision loss in wet age-related macular degeneration (wAMD) patients. Smoking not only aggravates the incidence and severity of the choroidal neovascularization of wAMD, but also affects the clinical treatment, making the prognosis worse. Nicotine, as an important harmful substance in tobacco, is an easily addictive and highly toxic alkaloid. Animal experiments and clinical studies have confirmed that nicotine can aggravate wAMD by mediating angiogenesis through nicotinic acetylcholine receptor, bone marrow blasts, inflammation, complement system, etc. Therefore, in order to early take appropriate intervention measures to prevent and delay the development, we should actively explore the exact pathogenesis by which nicotine aggravates the choroidal neovascularization.
Objective To investigate the correlation between the vitreomacular adhesion (VMA) and exudative age-related macular degeneration (AMD). Methods A literature research was performed in PubMed, EMbase, Cochrane Library, CNKI and Wanfang database from January 2000 to December 2016. Case-control studies on the relationship between VMA or posterior vitreous detachment and exudative AMD were included in this analysis. Literature screening and data extraction were performed according to inclusion and exclusion criteria. The qualities of the literatures were evaluated according to the Newcastle-Ottawa Scale (NOS). Seven literatures were selected into meta-analysis. The NOS score was 9 points in 1 article, 8 scores in 4 articles, 7 points in 2 articles. A total of 947 eyes with exudative AMD, 638 eyes with dry AMD, and 618 eyes with controls were included. The correlation between exudative AMD and VMA were analyzed using the software Review manager 5.3. Results The prevalence of VMA in exudative AMD eyes was higher than that in controls [odds ratio (OR)=2.14, 95% confidence interval (CI)=1.19 - 3.84, P=0.010] and dry AMD eyes (OR=2.24, 95%CI=1.24 - 4.03, P=0.007). There was no difference in PVD prevalence among exudative AMD eyes, dry AMD eyes (OR=0.44, 95%CI=0.16 - 1.20, P=0.110) and controls (OR=0.70, 95%CI=0.41 - 1.18, P=0.180). Conclusion There is correlation between VMA and exudative AMD.
MiRNAs are stable small RNAs that are expressed abundantly in animals and plants. They can bind to the 3'-untranslated region of the target mRNA, and regulate its expression at the post-transcriptional level. The miRNAs’ abnormal expression and its following abnormal biological regulation are closely related to the occurrence and development of age-related macular degeneration (AMD), including inflammatory response, oxidative stress injury, phagocytosis dysfunction and abnormal angiogenesis. Since the dysregulation of miR-155, miR-125b and miR-34a seems to play a more important role in AMD, these microRNAs may be expected to become the new biomarkers and therapeutic targets for AMD.
Purpose To detect whether a 3243 point mutation existed in age-related macular degeneration (AMD). MethodsTwenty-six cases of wet form AMD patients, ten cases of dry form AMD patients were selected,and compared with twenty nomal controls. After collecting anti-coagulated blood samples, total cellular DNA were extracted and purified. Using polymerase chain reaction and restriction fragment long polymorphism techniques, the mtDNA Ararr;G point mutation at position 3243 were detected. Results After cleaveded by restriction endonuclease Apa I, a 294 bp fragment remained only in all detected DNA samples including twenty-six wet form AMD, and ten dry form AMD. No any other fragment appeared. The result showed that there was no Ararr;G mutation at position 3243 found in AMD. Conclusion It is suggested that mtDNA 3243 point mutation due to maternal inheritance might be not concerned with both wet form AMD and dry form AMD. (Chin J Ocul Fundus Dis,2000,16:231-232)
Dysregulation and activation of immune processes are important in age-related macular degeneration (AMD) pathogenesis. The single nucleotide polymorphism of complement factor H is widely recognized as a risk factor to AMD. Over-activation of nod-like receptor3 and polymorphism of Toll-Like Receptor 3 also associated with AMD. Except for innate immune processes, adaptive immunity also play a critical role in AMD, a growing body of evidence supports that auto-antibodies and T cells are related with AMD. Additionally A2E and lipid oxidation byproducts might also have a role in AMD pathogenesis.