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      Fenofibrate for COVID-19 and related complications as an approach to improve treatment outcomes: the missed key for Holy Grail

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          Abstract

          Introduction

          Fenofibrate is an agonist of peroxisome proliferator activated receptor alpha (PPAR-α), that possesses anti-inflammatory, antioxidant, and anti-thrombotic properties. Fenofibrate is effective against a variety of viral infections and different inflammatory disorders. Therefore, the aim of critical review was to overview the potential role of fenofibrate in the pathogenesis of SARS-CoV-2 and related complications.

          Results

          By destabilizing SARS-CoV-2 spike protein and preventing it from binding angiotensin-converting enzyme 2 (ACE2), a receptor for SARS-CoV-2 entry, fenofibrate can reduce SARS-CoV-2 entry in human cells Fenofibrate also suppresses inflammatory signaling pathways, which decreases SARS-CoV-2 infection-related inflammatory alterations. In conclusion, fenofibrate anti-inflammatory, antioxidant, and antithrombotic capabilities may help to minimize the inflammatory and thrombotic consequences associated with SARSCoV-2 infection. Through attenuating the interaction between SARS-CoV-2 and ACE2, fenofibrate can directly reduce the risk of SARS-CoV-2 infection.

          Conclusions

          As a result, fenofibrate could be a potential treatment approach for COVID-19 control.

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          Cytokine Storm in COVID-19: The Current Evidence and Treatment Strategies

          Yujun Tang, Jiajia Liu, Dingyi Zhang … (2020)
          Severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2) is the pathogen that causes coronavirus disease 2019 (COVID-19). As of 25 May 2020, the outbreak of COVID-19 has caused 347,192 deaths around the world. The current evidence showed that severely ill patients tend to have a high concentration of pro-inflammatory cytokines, such as interleukin (IL)-6, compared to those who are moderately ill. The high level of cytokines also indicates a poor prognosis in COVID-19. Besides, excessive infiltration of pro-inflammatory cells, mainly involving macrophages and T-helper 17 cells, has been found in lung tissues of patients with COVID-19 by postmortem examination. Recently, increasing studies indicate that the “cytokine storm” may contribute to the mortality of COVID-19. Here, we summarize the clinical and pathologic features of the cytokine storm in COVID-19. Our review shows that SARS-Cov-2 selectively induces a high level of IL-6 and results in the exhaustion of lymphocytes. The current evidence indicates that tocilizumab, an IL-6 inhibitor, is relatively effective and safe. Besides, corticosteroids, programmed cell death protein (PD)-1/PD-L1 checkpoint inhibition, cytokine-adsorption devices, intravenous immunoglobulin, and antimalarial agents could be potentially useful and reliable approaches to counteract cytokine storm in COVID-19 patients.
          Article 0 comments Cited 536 times – based on 0 reviews     Review now
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            Endothelial dysfunction and immunothrombosis as key pathogenic mechanisms in COVID-19

            Aldo Bonaventura, Alessandra Vecchié, Lorenzo Dagna … (2021)
            Coronavirus disease 2019 (COVID-19) is a clinical syndrome caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Patients with severe disease show hyperactivation of the immune system, which can affect multiple organs besides the lungs. Here, we propose that SARS-CoV-2 infection induces a process known as immunothrombosis, in which activated neutrophils and monocytes interact with platelets and the coagulation cascade, leading to intravascular clot formation in small and larger vessels. Microthrombotic complications may contribute to acute respiratory distress syndrome (ARDS) and other organ dysfunctions. Therapeutic strategies aimed at reducing immunothrombosis may therefore be useful. Several antithrombotic and immunomodulating drugs have been proposed as candidates to treat patients with SARS-CoV-2 infection. The growing understanding of SARS-CoV-2 infection pathogenesis and how it contributes to critical illness and its complications may help to improve risk stratification and develop targeted therapies to reduce the acute and long-term consequences of this disease.
            Article 0 comments Cited 380 times – based on 0 reviews     Review now
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              Effects of long-term fenofibrate therapy on cardiovascular events in 9795 people with type 2 diabetes mellitus (the FIELD study): randomised controlled trial.

              A. Keech, R Simes, P Barter … (2005)
              Patients with type 2 diabetes mellitus are at increased risk of cardiovascular disease, partly owing to dyslipidaemia, which can be amenable to fibrate therapy. We designed the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study to assess the effect of fenofibrate on cardiovascular disease events in these patients. We did a multinational, randomised controlled trial with 9795 participants aged 50-75 years, with type 2 diabetes mellitus, and not taking statin therapy at study entry. After a placebo and a fenofibrate run-in phase, we randomly assigned patients (2131 with previous cardiovascular disease and 7664 without) with a total-cholesterol concentration of 3.0-6.5 mmol/L and a total-cholesterol/HDL-cholesterol ratio of 4.0 or more or plasma triglyceride of 1.0-5.0 mmol/L to micronised fenofibrate 200 mg daily (n=4895) or matching placebo (n=4900). Our primary outcome was coronary events (coronary heart disease death or non-fatal myocardial infarction); the outcome for prespecified subgroup analyses was total cardiovascular events (the composite of cardiovascular death, myocardial infarction, stroke, and coronary and carotid revascularisation). Analysis was by intention to treat. The study was prospectively registered (number ISRCTN 64783481). Vital status was confirmed on all but 22 patients. Averaged over the 5 years' study duration, similar proportions in each group discontinued study medication (10% placebo vs 11% fenofibrate) and more patients allocated placebo (17%) than fenofibrate (8%; p<0.0001) commenced other lipid treatments, predominantly statins. 5.9% (n=288) of patients on placebo and 5.2% (n=256) of those on fenofibrate had a coronary event (relative reduction of 11%; hazard ratio [HR] 0.89, 95% CI 0.75-1.05; p=0.16). This finding corresponds to a significant 24% reduction in non-fatal myocardial infarction (0.76, 0.62-0.94; p=0.010) and a non-significant increase in coronary heart disease mortality (1.19, 0.90-1.57; p=0.22). Total cardiovascular disease events were significantly reduced from 13.9% to 12.5% (0.89, 0.80-0.99; p=0.035). This finding included a 21% reduction in coronary revascularisation (0.79, 0.68-0.93; p=0.003). Total mortality was 6.6% in the placebo group and 7.3% in the fenofibrate group (p=0.18). Fenofibrate was associated with less albuminuria progression (p=0.002), and less retinopathy needing laser treatment (5.2%vs 3.6%, p=0.0003). There was a slight increase in pancreatitis (0.5%vs 0.8%, p=0.031) and pulmonary embolism (0.7%vs 1.1%, p=0.022), but no other significant adverse effects. Fenofibrate did not significantly reduce the risk of the primary outcome of coronary events. It did reduce total cardiovascular events, mainly due to fewer non-fatal myocardial infarctions and revascularisations. The higher rate of starting statin therapy in patients allocated placebo might have masked a moderately larger treatment benefit.
              Article 0 comments Cited 206 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Shadi Salem Alkhayyat: DR_shadi2002@hotmail.com
                Hayder M. Al-kuraishy: Hayderm36@yahoo.com
                Ali I. Al-Gareeb: Dr.alialgareeb78@yahoo.com
                Maisra M. El-Bouseary: maysra_mohamed@pharm.tanta.edu.eg
                Amal M. AboKamer: amalabokamer@pharm.tanta.edu.eg
                Gaber El-Saber Batiha: gaberbatiha@gmail.com
                Jesus Simal-Gandara: jsimal@uvigo.es
                Journal
                Journal ID (nlm-ta): Inflamm Res
                Journal ID (iso-abbrev): Inflamm Res
                Title: Inflammation Research
                Publisher: Springer International Publishing (Cham )
                ISSN (Print): 1023-3830
                ISSN (Electronic): 1420-908X
                Publication date (Electronic): 8 August 2022
                Pages: 1-9
                Affiliations
                [1 ]GRID grid.412125.1, ISNI 0000 0001 0619 1117, Department of Internal Medicine, Faculty of Medicine, , King Abdulaziz University, ; Jeddah, 21589 Saudi Arabia
                [2 ]GRID grid.411309.e, ISNI 0000 0004 1765 131X, Department of Clinical Pharmacology and Medicine, College of Medicine, , Al-Mustansiriyah University, ; Baghdad, Iraq
                [3 ]GRID grid.412258.8, ISNI 0000 0000 9477 7793, Department of Pharmaceutical Microbiology, Faculty of Pharmacy, , Tanta University, ; Tanta, Egypt
                [4 ]GRID grid.449014.c, ISNI 0000 0004 0583 5330, Department of Pharmacology and Therapeutics, Faculty of Veterinary Medicine, , Damanhour University, ; Damanhour, 22511 Al Beheira Egypt
                [5 ]GRID grid.6312.6, ISNI 0000 0001 2097 6738, Nutrition and Bromatology Group, Department of Analytical Chemistry and Food Science, Faculty Science, , Universidade de Vigo, ; 32004 Ourense, Spain
                Article
                Publisher ID: 1615
                DOI: 10.1007/s00011-022-01615-w
                PMC ID: 9360649
                PubMed ID: 35941297
                SO-VID: 76bbb9d1-a020-45ec-8bae-c6498f1cb7e7
                Copyright © © The Author(s), under exclusive licence to Springer Nature Switzerland AG 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 : 13 May 2022
                Date revision received : 5 July 2022
                Date accepted : 17 July 2022
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100006761, Universidade de Vigo;
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                Categories
                Subject: Review

                ScienceOpen disciplines: Immunology
                Keywords: fenofibrate,covid-19,sars-cov-2,angiotensin-converting enzyme 2
                Data availability:
                ScienceOpen disciplines: Immunology
                Keywords: fenofibrate, covid-19, sars-cov-2, angiotensin-converting enzyme 2

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