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      Evaluation of Systemic Renin and Angiotensin II Levels in Normal Tension Glaucoma

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          Abstract

          The purpose of this study was to investigate the function of the renin–angiotensin–aldosterone system (RAAS) in normal tension glaucoma (NTG) patients by measuring the level of renin and angiotensin II (AngII) in the plasma. Twenty-four patients with NTG and 38 control subjects were included in this study. Renin and AngII were measured in the blood samples of all subjects by enzyme-linked immunosorbent assay (ELISA). No significant differences were found in the complete blood count, fasting glucose, low-density lipoprotein (LDL), and high-sensitivity C-reactive protein (hs-CRP) levels between the control and NTG groups. The systemic concentration and variability of the renin concentration in the blood was significantly higher in the NTG group ( p = 0.005 and 0.005, respectively). According to multivariate logistic regression analysis, the variability of the renin concentration was associated with NTG ( p = 0.006). In conclusion, the systemic concentration and variability of renin levels were elevated in NTG patients. An altered renin concentration could represent a difference in RAAS function in NTG patients.

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          Most cited references37

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          Primary open-angle glaucoma.

          Primary open-angle glaucoma is a progressive optic neuropathy and, perhaps, the most common form of glaucoma. Because the disease is treatable, and because the visual impairment caused by glaucoma is irreversible, early detection is essential. Early diagnosis depends on examination of the optic disc, retinal nerve fibre layer, and visual field. New imaging and psychophysical tests can improve both detection and monitoring of the progression of the disease. Recently completed long-term clinical trials provide convincing evidence that lowering intraocular pressure prevents progression at both the early and late stages of the disease. The degree of protection is related to the degree to which intraocular pressure is lowered. Improvements in therapy consist of more effective and better-tolerated drugs to lower intraocular pressure, and more effective surgical procedures. New treatments to directly treat and protect the retinal ganglion cells that are damaged in glaucoma are also in development.
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            The Renin-Angiotensin-Aldosterone System in Vascular Inflammation and Remodeling

            The RAAS through its physiological effectors plays a key role in promoting and maintaining inflammation. Inflammation is an important mechanism in the development and progression of CVD such as hypertension and atherosclerosis. In addition to its main role in regulating blood pressure and its role in hypertension, RAAS has proinflammatory and profibrotic effects at cellular and molecular levels. Blocking RAAS provides beneficial effects for the treatment of cardiovascular and renal diseases. Evidence shows that inhibition of RAAS positively influences vascular remodeling thus improving CVD outcomes. The beneficial vascular effects of RAAS inhibition are likely due to decreasing vascular inflammation, oxidative stress, endothelial dysfunction, and positive effects on regeneration of endothelial progenitor cells. Inflammatory factors such as ICAM-1, VCAM-1, TNFα, IL-6, and CRP have key roles in mediating vascular inflammation and blocking RAAS negatively modulates the levels of these inflammatory molecules. Some of these inflammatory markers are clinically associated with CVD events. More studies are required to establish long-term effects of RAAS inhibition on vascular inflammation, vascular cells regeneration, and CVD clinical outcomes. This review presents important information on RAAS's role on vascular inflammation, vascular cells responses to RAAS, and inhibition of RAAS signaling in the context of vascular inflammation, vascular remodeling, and vascular inflammation-associated CVD. Nevertheless, the review also equates the need to rethink and rediscover new RAAS inhibitors.
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              Neuroinflammation in glaucoma: A new opportunity.

              Mounting evidence suggests neuroinflammation is a key process in glaucoma, yet the precise roles are not known. Understanding these complex processes, which may also be a key in other common neurodegenerations such as Alzheimer's disease, will lead to targeted therapeutics for a disease that affects as many as 80 million people worldwide. Here, we define neuroinflammation as any immune-relevant response by a variety of cell types including astrocytes, microglia, and peripherally derived cells occurring in the optic nerve head and/or retina. In this review article, we first discuss clinical evidence for neuroinflammation in glaucoma and define neuroinflammation in glaucoma. We then review the inflammatory pathways that have been associated with glaucoma. Finally, we set out key research directions that we believe will greatly advance our understanding of the role of neuroinflammation in glaucoma. This review arose from a discussion of neuroinflammation in glaucoma at the 2015 meeting of The Lasker/IRRF Initiative for Innovation in Vision Science. This manuscript sets out to summarize one of these sessions; "Inflammation and Glaucomatous Neurodegeneration", as well as to review the current state of the literature surrounding neuroinflammation in glaucoma.
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                Author and article information

                Journal
                J Clin Med
                J Clin Med
                jcm
                Journal of Clinical Medicine
                MDPI
                2077-0383
                26 November 2020
                December 2020
                : 9
                : 12
                : 3838
                Affiliations
                [1 ]Department of Ophthalmology, Eunpyeong St. Mary’s Hospital, College of Medicine, The Catholic University of Korea, Seoul 03312, Korea; sj8801@ 123456gmail.com
                [2 ]Department of Ophthalmology, Incheon St. Mary’s Hospital, College of Medicine, The Catholic University of Korea, Incheon 21431, Korea; leoanzel@ 123456catholic.ac.kr
                Author notes
                [* ]Correspondence: nyny5555@ 123456naver.com ; Tel.: +82-2-2030-2795; Fax: +82-2-599-7405
                Author information
                https://orcid.org/0000-0002-3284-4756
                Article
                jcm-09-03838
                10.3390/jcm9123838
                7761439
                33256138
                93ed162c-f6d0-4b4c-abeb-85894e234040
                © 2020 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 27 October 2020
                : 24 November 2020
                Categories
                Article

                renin,angiotensin ii,normal tension glaucoma,renin–angiotensin–aldosterone system

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