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      Potential of the Angiotensin Receptor Blockers (ARBs) Telmisartan, Irbesartan, and Candesartan for Inhibiting the HMGB1/RAGE Axis in Prevention and Acute Treatment of Stroke

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          Abstract

          Stroke is a major cause of mortality and disability worldwide. The main cause of stroke is atherosclerosis, and the most common risk factor for atherosclerosis is hypertension. Therefore, antihypertensive treatments are recommended for the prevention of stroke. Three angiotensin receptor blockers (ARBs), telmisartan, irbesartan and candesartan, inhibit the expression of the receptor for advanced glycation end-products (RAGE), which is one of the pleiotropic effects of these drugs. High mobility group box 1 (HMGB1) is the ligand of RAGE, and has been recently identified as a lethal mediator of severe sepsis. HMGB1 is an intracellular protein, which acts as an inflammatory cytokine when released into the extracellular milieu. Extracellular HMGB1 causes multiple organ failure and contributes to the pathogenesis of hypertension, hyperlipidemia, diabetes mellitus, atherosclerosis, thrombosis, and stroke. This is the first review of the literature evaluating the potential of three ARBs for the HMGB1-RAGE axis on stroke therapy, including prevention and acute treatment. This review covers clinical and experimental studies conducted between 1976 and 2013. We propose that ARBs, which inhibit the HMGB1/RAGE axis, may offer a novel option for prevention and acute treatment of stroke. However, additional clinical studies are necessary to verify the efficacy of ARBs.

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          HMG-1 as a late mediator of endotoxin lethality in mice.

          H. Wang, O Bloom, M. Zhang … (1999)
          Endotoxin, a constituent of Gram-negative bacteria, stimulates macrophages to release large quantities of tumor necrosis factor (TNF) and interleukin-1 (IL-1), which can precipitate tissue injury and lethal shock (endotoxemia). Antagonists of TNF and IL-1 have shown limited efficacy in clinical trials, possibly because these cytokines are early mediators in pathogenesis. Here a potential late mediator of lethality is identified and characterized in a mouse model. High mobility group-1 (HMG-1) protein was found to be released by cultured macrophages more than 8 hours after stimulation with endotoxin, TNF, or IL-1. Mice showed increased serum levels of HMG-1 from 8 to 32 hours after endotoxin exposure. Delayed administration of antibodies to HMG-1 attenuated endotoxin lethality in mice, and administration of HMG-1 itself was lethal. Septic patients who succumbed to infection had increased serum HMG-1 levels, suggesting that this protein warrants investigation as a therapeutic target.
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            Guidelines for the prevention of stroke in patients with stroke or transient ischemic attack: a guideline for healthcare professionals from the american heart association/american stroke association.

            Karen Furie, Scott E Kasner, Robert J. Adams … (2011)
            The aim of this updated statement is to provide comprehensive and timely evidence-based recommendations on the prevention of ischemic stroke among survivors of ischemic stroke or transient ischemic attack. Evidence-based recommendations are included for the control of risk factors, interventional approaches for atherosclerotic disease, antithrombotic treatments for cardioembolism, and the use of antiplatelet agents for noncardioembolic stroke. Further recommendations are provided for the prevention of recurrent stroke in a variety of other specific circumstances, including arterial dissections; patent foramen ovale; hyperhomocysteinemia; hypercoagulable states; sickle cell disease; cerebral venous sinus thrombosis; stroke among women, particularly with regard to pregnancy and the use of postmenopausal hormones; the use of anticoagulation after cerebral hemorrhage; and special approaches to the implementation of guidelines and their use in high-risk populations.
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              Pathobiology of ischaemic stroke: an integrated view.

              C Iadecola, M Moskowitz (1999)
              Brain injury following transient or permanent focal cerebral ischaemia (stroke) develops from a complex series of pathophysiological events that evolve in time and space. In this article, the relevance of excitotoxicity, peri-infarct depolarizations, inflammation and apoptosis to delayed mechanisms of damage within the peri-infarct zone or ischaemic penumbra are discussed. While focusing on potentially new avenues of treatment, the issue of why many clinical stroke trials have so far proved disappointing is addressed. This article provides a framework that can be used to generate testable hypotheses and treatment strategies that are linked to the appearance of specific pathophysiological events within the ischaemic brain.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Mol Sci
                Journal ID (iso-abbrev): Int J Mol Sci
                Journal ID (publisher-id): ijms
                Title: International Journal of Molecular Sciences
                Publisher: Molecular Diversity Preservation International (MDPI)
                ISSN (Electronic): 1422-0067
                Publication date Collection: September 2013
                Publication date (Electronic): 13 September 2013
                Volume: 14
                Issue: 9
                Pages: 18899-18924
                Affiliations
                [1 ]Department of Pharmacology, Faculty of Dentistry, Mahidol University, 6 Yothe Road, Rajthevee, Bangkok 10400, Thailand; E-Mails: kikuchi_kiyoshi@ 123456kurume-u.ac.jp (K.K.); salunya.tan@ 123456mahidol.ac.th (S.T.)
                [2 ]Division of Brain Science, Department of Physiology, Kurume University School of Medicine, 67 Asahi-machi, Kurume 830-0011, Japan; E-Mail: ymurai@ 123456med.kurume-u.ac.jp
                [3 ]Department of Neurosurgery, Kurume University School of Medicine, 67 Asahi-machi, Kurume 830-0011, Japan
                [4 ]Department of Systems Biology in Thromboregulation, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1 Sakuragaoka, Kagoshima 890-8520, Japan; E-Mails: takashi@ 123456m3.kufm.kagoshima-u.ac.jp (T.I.); rinken@ 123456m3.kufm.kagoshima-u.ac.jp (I.M.)
                [5 ]Department of Restorative Dentistry and Endodontology, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1 Sakuragaoka, Kagoshima 890-8544, Japan; E-Mail: yokomaru@ 123456dent.kagoshima-u.ac.jp
                [6 ]Laboratory of Diagnostic Imaging, Department of Veterinary Science, Faculty of Agriculture, Kagoshima University, 1-21-24 Korimoto, Kagoshima 890-0065, Japan; E-Mail: nm18@ 123456vet.kagoshima-u.ac.jp
                [7 ]Laboratory of Functional Foods, Department of Biomedical Engineering Osaka Institute of Technology, 5-16-1 Omiya, Asahi Ward, Osaka 535-8585, Japan; E-Mail: kawahara@ 123456bme.oit.ac.jp
                Author notes
                [* ]Author to whom correspondence should be addressed; E-Mail: eacht@ 123456med.kurume-u.ac.jp ; Tel.: +81-942-31-7542; Fax: +81-942-31-7695.
                Article
                Publisher ID: ijms-14-18899
                DOI: 10.3390/ijms140918899
                PMC ID: 3794813
                PubMed ID: 24065095
                SO-VID: c3255272-31f1-4639-a2b2-bf07cf7bc301
                Copyright © © 2013 by the authors; licensee MDPI, Basel, Switzerland
                License:

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/3.0/).

                History
                Date received : 15 August 2013
                Date revision received : 07 September 2013
                Date accepted : 09 September 2013
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular biology
                Keywords: stroke,telmisartan,irbesartan,candesartan,high mobility group box 1,receptor for advanced glycation end-products
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: stroke, telmisartan, irbesartan, candesartan, high mobility group box 1, receptor for advanced glycation end-products

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