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Brief Report

An Insight into Giant Cell Arteritis Pathogenesis: Evidence for Oxidative Stress and SIRT1 Downregulation

1
Department of Cardiac Development and Remodeling, Max-Planck-Institute for Heart and Lung Research, Ludwigstrasse 43, 61231 Bad Nauheim, Germany
2
Department of Experimental and Clinical Biomedical Sciences “Mario Serio”, University of Firenze, 50134 Firenze, Italy
3
Department of Experimental and Clinical Medicine, University of Firenze, 50134 Firenze, Italy
*
Author to whom correspondence should be addressed.
Academic Editor: Stanley Omaye
Antioxidants 2021, 10(6), 885; https://doi.org/10.3390/antiox10060885
Received: 30 April 2021 / Revised: 26 May 2021 / Accepted: 27 May 2021 / Published: 31 May 2021
Giant cell arteritis (GCA), medium and large vessel granulomatous vasculitis affecting the elderly, is characterized by a multitude of vascular complications, including venous thrombosis, myocardial infraction and stroke. The formation of granulomatous infiltrates and the enhanced accumulation of proinflammatory cytokines are typical features of this condition. The GCA pathogenesis remains largely unknown, but recent studies have suggested the involvement of oxidative stress, mainly sustained by an enhanced reactive oxygen species (ROS) production by immature neutrophils. On this basis, in the present study, we intended to evaluate, in GCA patients, the presence of systemic oxidative stress and possible alterations in the expression level of nuclear sirtuins, enzymes involved in the inhibition of inflammation and oxidative stress. Thirty GCA patients were included in the study and compared to 30 healthy controls in terms of leukocyte ROS production, oxidative stress and SIRT1 expression. Our results clearly indicated a significant increase (p < 0.05) both in the ROS levels in the leukocyte fractions and plasma oxidative stress markers (lipid peroxidation and total antioxidant capacity) in the GCA patients compared to the healthy controls. In PBMCs from the GCA patients, a significant decrease in SIRT1 expression (p < 0.05) but not in SIRT6 and SIRT7 expression was found. Taken together, our preliminary findings indicate that, in GCA patients, plasma oxidative stress is paralleled by a reduced SIRT1 expression in PBMC. Further studies are needed to highlight if and how these alterations contribute to GCA pathogenesis. View Full-Text
Keywords: giant cell arteritis (GCA); oxidative stress; SIRT1 giant cell arteritis (GCA); oxidative stress; SIRT1
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MDPI and ACS Style

Ianni, A.; Kumari, P.; Tarighi, S.; Argento, F.R.; Fini, E.; Emmi, G.; Bettiol, A.; Braun, T.; Prisco, D.; Fiorillo, C.; Becatti, M. An Insight into Giant Cell Arteritis Pathogenesis: Evidence for Oxidative Stress and SIRT1 Downregulation. Antioxidants 2021, 10, 885. https://doi.org/10.3390/antiox10060885

AMA Style

Ianni A, Kumari P, Tarighi S, Argento FR, Fini E, Emmi G, Bettiol A, Braun T, Prisco D, Fiorillo C, Becatti M. An Insight into Giant Cell Arteritis Pathogenesis: Evidence for Oxidative Stress and SIRT1 Downregulation. Antioxidants. 2021; 10(6):885. https://doi.org/10.3390/antiox10060885

Chicago/Turabian Style

Ianni, Alessandro, Poonam Kumari, Shahriar Tarighi, Flavia Rita Argento, Eleonora Fini, Giacomo Emmi, Alessandra Bettiol, Thomas Braun, Domenico Prisco, Claudia Fiorillo, and Matteo Becatti. 2021. "An Insight into Giant Cell Arteritis Pathogenesis: Evidence for Oxidative Stress and SIRT1 Downregulation" Antioxidants 10, no. 6: 885. https://doi.org/10.3390/antiox10060885

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