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      The Remarkable Roles of the Receptor for Advanced Glycation End Products (RAGE) and Its Soluble Isoforms in COVID-19: The Importance of RAGE Pathway in the Lung Injuries

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          Abstract

          The respiratory symptoms of acute respiratory distress syndrome (ARDS) in the coronavirus disease 2019 (COVID-19) patients is associated with accumulation of pre-inflammatory molecules such as advanced glycation end-products (AGES), calprotectin, high mobility group box family-1 (HMGB1), cytokines, angiotensin converting enzyme 2 (ACE2), and other molecules in the alveolar space of lungs and plasma. The receptor for advanced glycation end products (RAGEs), which is mediated by the mitogen-activated protein kinase (MAPK), plays a critical role in the severity of chronic inflammatory diseases such as diabetes mellitus (DM) and ARDS. The RAGE gene is most expressed in the alveolar epithelial cells (AECs) of the pulmonary system. Several clinical trials are now being conducted to determine the possible association between the levels of soluble isoforms of RAGE (sRAGE and esRAGE) and the severity of the disease in patients with ARDS and acute lung injury (ALI). In the current article, we reviewed the most recent studies on the RAGE/ligands axis and sRAGE/esRAGE levels in acute respiratory illness, with a focus on COVID-19–associated ARDS (CARDS) patients. According to the research conducted so far, sRAGE/esRAGE measurements in patients with CARDS can be used as a powerful chemical indicator among other biomarkers for assessment of early pulmonary involvement. Furthermore, inhibiting RAGE/MAPK and Angiotensin II receptor type 1 (ATR1) in CARDS patients can be a powerful strategy for diminishing cytokine storm and severe respiratory symptoms.

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          Remdesivir for the Treatment of Covid-19 — Final Report

          John H. Beigel, Kay Tomashek, Lori Dodd … (2022)
          Abstract Background Although several therapeutic agents have been evaluated for the treatment of coronavirus disease 2019 (Covid-19), none have yet been shown to be efficacious. Methods We conducted a double-blind, randomized, placebo-controlled trial of intravenous remdesivir in adults hospitalized with Covid-19 with evidence of lower respiratory tract involvement. Patients were randomly assigned to receive either remdesivir (200 mg loading dose on day 1, followed by 100 mg daily for up to 9 additional days) or placebo for up to 10 days. The primary outcome was the time to recovery, defined by either discharge from the hospital or hospitalization for infection-control purposes only. Results A total of 1063 patients underwent randomization. The data and safety monitoring board recommended early unblinding of the results on the basis of findings from an analysis that showed shortened time to recovery in the remdesivir group. Preliminary results from the 1059 patients (538 assigned to remdesivir and 521 to placebo) with data available after randomization indicated that those who received remdesivir had a median recovery time of 11 days (95% confidence interval [CI], 9 to 12), as compared with 15 days (95% CI, 13 to 19) in those who received placebo (rate ratio for recovery, 1.32; 95% CI, 1.12 to 1.55; P<0.001). The Kaplan-Meier estimates of mortality by 14 days were 7.1% with remdesivir and 11.9% with placebo (hazard ratio for death, 0.70; 95% CI, 0.47 to 1.04). Serious adverse events were reported for 114 of the 541 patients in the remdesivir group who underwent randomization (21.1%) and 141 of the 522 patients in the placebo group who underwent randomization (27.0%). Conclusions Remdesivir was superior to placebo in shortening the time to recovery in adults hospitalized with Covid-19 and evidence of lower respiratory tract infection. (Funded by the National Institute of Allergy and Infectious Diseases and others; ACTT-1 ClinicalTrials.gov number, NCT04280705.)
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            Efficacy and safety of nintedanib in idiopathic pulmonary fibrosis.

            Luca Richeldi, Roland M du Bois, Ganesh Raghu … (2014)
            Nintedanib (formerly known as BIBF 1120) is an intracellular inhibitor that targets multiple tyrosine kinases. A phase 2 trial suggested that treatment with 150 mg of nintedanib twice daily reduced lung-function decline and acute exacerbations in patients with idiopathic pulmonary fibrosis. We conducted two replicate 52-week, randomized, double-blind, phase 3 trials (INPULSIS-1 and INPULSIS-2) to evaluate the efficacy and safety of 150 mg of nintedanib twice daily as compared with placebo in patients with idiopathic pulmonary fibrosis. The primary end point was the annual rate of decline in forced vital capacity (FVC). Key secondary end points were the time to the first acute exacerbation and the change from baseline in the total score on the St. George's Respiratory Questionnaire, both assessed over a 52-week period. A total of 1066 patients were randomly assigned in a 3:2 ratio to receive nintedanib or placebo. The adjusted annual rate of change in FVC was -114.7 ml with nintedanib versus -239.9 ml with placebo (difference, 125.3 ml; 95% confidence interval [CI], 77.7 to 172.8; P<0.001) in INPULSIS-1 and -113.6 ml with nintedanib versus -207.3 ml with placebo (difference, 93.7 ml; 95% CI, 44.8 to 142.7; P<0.001) in INPULSIS-2. In INPULSIS-1, there was no significant difference between the nintedanib and placebo groups in the time to the first acute exacerbation (hazard ratio with nintedanib, 1.15; 95% CI, 0.54 to 2.42; P=0.67); in INPULSIS-2, there was a significant benefit with nintedanib versus placebo (hazard ratio, 0.38; 95% CI, 0.19 to 0.77; P=0.005). The most frequent adverse event in the nintedanib groups was diarrhea, with rates of 61.5% and 18.6% in the nintedanib and placebo groups, respectively, in INPULSIS-1 and 63.2% and 18.3% in the two groups, respectively, in INPULSIS-2. In patients with idiopathic pulmonary fibrosis, nintedanib reduced the decline in FVC, which is consistent with a slowing of disease progression; nintedanib was frequently associated with diarrhea, which led to discontinuation of the study medication in less than 5% of patients. (Funded by Boehringer Ingelheim; INPULSIS-1 and INPULSIS-2 ClinicalTrials.gov numbers, NCT01335464 and NCT01335477.).
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              SARS-CoV-2 Neutralizing Antibody LY-CoV555 in Outpatients with Covid-19

              Peter Chen, Ajay Nirula, Barry Heller … (2020)
              Abstract Background Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus disease 2019 (Covid-19), which is most frequently mild yet can be severe and life-threatening. Virus-neutralizing monoclonal antibodies are predicted to reduce viral load, ameliorate symptoms, and prevent hospitalization. Methods In this ongoing phase 2 trial involving outpatients with recently diagnosed mild or moderate Covid-19, we randomly assigned 452 patients to receive a single intravenous infusion of neutralizing antibody LY-CoV555 in one of three doses (700 mg, 2800 mg, or 7000 mg) or placebo and evaluated the quantitative virologic end points and clinical outcomes. The primary outcome was the change from baseline in the viral load at day 11. The results of a preplanned interim analysis as of September 5, 2020, are reported here. Results At the time of the interim analysis, the observed mean decrease from baseline in the log viral load for the entire population was −3.81, for an elimination of more than 99.97% of viral RNA. For patients who received the 2800-mg dose of LY-CoV555, the difference from placebo in the decrease from baseline was −0.53 (95% confidence interval [CI], −0.98 to −0.08; P=0.02), for a viral load that was lower by a factor of 3.4. Smaller differences from placebo in the change from baseline were observed among the patients who received the 700-mg dose (−0.20; 95% CI, −0.66 to 0.25; P=0.38) or the 7000-mg dose (0.09; 95% CI, −0.37 to 0.55; P=0.70). On days 2 to 6, the patients who received LY-CoV555 had a slightly lower severity of symptoms than those who received placebo. The percentage of patients who had a Covid-19–related hospitalization or visit to an emergency department was 1.6% in the LY-CoV555 group and 6.3% in the placebo group. Conclusions In this interim analysis of a phase 2 trial, one of three doses of neutralizing antibody LY-CoV555 appeared to accelerate the natural decline in viral load over time, whereas the other doses had not by day 11. (Funded by Eli Lilly; BLAZE-1 ClinicalTrials.gov number, NCT04427501.)
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                Author and article information

                Contributors
                Mitra Salehi:
                ORCID: http://orcid.org/0000-0001-8061-1255
                m.salehi@qums.ac.ir , mitra.salehi1374@gmail.com
                Shahin Amiri:
                ORCID: http://orcid.org/0000-0003-0596-2076
                sh_amiri@pasteur.ac.ir , shaahinamiri@gmail.com
                Dariush Ilghari: d.ilghari@gmail.com
                Hossein Piri:
                ORCID: http://orcid.org/0000-0001-8402-7742
                hpiri@qums.ac.ir , hosseinpiry@gmail.com
                Journal
                Journal ID (nlm-ta): Indian J Clin Biochem
                Journal ID (iso-abbrev): Indian J Clin Biochem
                Title: Indian Journal of Clinical Biochemistry
                Publisher: Springer India (New Delhi )
                ISSN (Print): 0970-1915
                ISSN (Electronic): 0974-0422
                Publication date (Electronic): 18 August 2022
                Pages: 1-13
                Affiliations
                [1 ]GRID grid.412606.7, ISNI 0000 0004 0405 433X, Student Research Committee, , Qazvin University of Medical Sciences, ; Qazvin, Iran
                [2 ]GRID grid.420169.8, ISNI 0000 0000 9562 2611, Department of Medical Biotechnology, Biotechnology Research Center, , Pasteur Institute of Iran, ; Tehran, Iran
                [3 ]GRID grid.420169.8, ISNI 0000 0000 9562 2611, Student Research Committee, , Pasteur Institute of Iran, ; Tehran, Iran
                [4 ]GRID grid.51462.34, ISNI 0000 0001 2171 9952, Midland Memorial Hospital, ; 400 Rosalind Redfern Grover Pkwy, Midland, TX 79701 USA
                [5 ]GRID grid.412606.7, ISNI 0000 0004 0405 433X, Department of Biochemistry and Genetics, School of Medicine, , Qazvin University of Medical Sciences, ; Qazvin, Iran
                [6 ]GRID grid.412606.7, ISNI 0000 0004 0405 433X, Cellular and Molecular Research Center, , Research Institute for Prevention of Non Communicable Diseases, Qazvin University of Medical Sciences, ; Qazvin, Iran
                Author information
                http://orcid.org/0000-0001-8061-1255
                http://orcid.org/0000-0003-0596-2076
                http://orcid.org/0000-0001-8402-7742
                Article
                Publisher ID: 1081
                DOI: 10.1007/s12291-022-01081-5
                PMC ID: 9387879
                PubMed ID: 35999871
                SO-VID: ac7cc469-7f12-4612-8de2-0b6cc6fc86e8
                Copyright © © The Author(s), under exclusive licence to Association of Clinical Biochemists of India 2022, Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.
                License:

                This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.

                History
                Date received : 22 April 2022
                Date accepted : 22 July 2022
                Categories
                Subject: Review Article

                Keywords: receptor for advanced glycation end products,sars-cov- 2,respiratory distress syndrome,esrage,ace2 protein
                Data availability:
                Keywords: receptor for advanced glycation end products, sars-cov- 2, respiratory distress syndrome, esrage, ace2 protein

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