Tales Lyra Oliveira1,2, Igor Santana Melo3, Léia Cardoso-Sousa4, Igor Andrade Santos5, Mohamad Bassim El Zoghbi2, Caroline Gusson Shimoura6, Renata Pereira Georjutti6, Olagide Wagner Castro3, Luiz Ricardo Goulart7,8, Ana Carolina Gomes Jardim5, Thúlio Marquez Cunha9, Robinson Sabino-Silva4. 1. Heart Institute, Faculty of Medicine, University of São Paulo, São Paulo, Brazil. 2. Medical School, Municipal University of São Caetano do Sul, São Paulo, Brazil. 3. Institute of Biological Sciences and Health, Federal University of Alagoas, Alagoas, Brazil. 4. Department of Physiology, Institute of Biomedical Sciences, Federal University of Uberlândia, Uberlândia, Brazil. 5. Laboratory of Virology, Institute of Biomedical Sciences, Federal University of Uberlândia, Uberlândia, Brazil. 6. Department of Physiology and Anatomy, University of North Texas Health Science Center, Fort Worth, TX, United States. 7. Institute of Biotechnology, Federal University of Uberlândia, Uberlândia, Brazil. 8. Department of Medical Microbiology and Immunology, University of California, Davis, Davis, CA, United States. 9. Department of Pulmonology, School of Medicine, Federal University of Uberlândia, Uberlândia, Brazil.
Abstract
Novel coronavirus disease (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Its impact on patients with comorbidities is clearly related to fatality cases, and diabetes has been linked to one of the most important causes of severity and mortality in SARS-CoV-2 infected patients. Substantial research progress has been made on COVID-19 therapeutics; however, effective treatments remain unsatisfactory. This unmet clinical need is robustly associated with the complexity of pathophysiological mechanisms described for COVID-19. Several key lung pathophysiological mechanisms promoted by SARS-CoV-2 have driven the response in normoglycemic and hyperglycemic subjects. There is sufficient evidence that glucose metabolism pathways in the lung are closely tied to bacterial proliferation, inflammation, oxidative stress, and pro-thrombotic responses, which lead to severe clinical outcomes. It is also likely that SARS-CoV-2 proliferation is affected by glucose metabolism of type I and type II cells. This review summarizes the current understanding of pathophysiology of SARS-CoV-2 in the lung of diabetic patients and highlights the changes in clinical outcomes of COVID-19 in normoglycemic and hyperglycemic conditions.
Novel coronavirus disease (n class="Disease">COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Its impact on patients with comorbidities is clearly related to fatality cases, and diabetes has been linked to one of the most important causes of severity and mortality in SARS-CoV-2 infectedpatients. Substantial research progress has been made on COVID-19 therapeutics; however, effective treatments remain unsatisfactory. This unmet clinical need is robustly associated with the complexity of pathophysiological mechanisms described for COVID-19. Several key lung pathophysiological mechanisms promoted by SARS-CoV-2 have driven the response in normoglycemic and hyperglycemic subjects. There is sufficient evidence that glucose metabolism pathways in the lung are closely tied to bacterial proliferation, inflammation, oxidative stress, and pro-thrombotic responses, which lead to severe clinical outcomes. It is also likely that SARS-CoV-2 proliferation is affected by glucose metabolism of type I and type II cells. This review summarizes the current understanding of pathophysiology of SARS-CoV-2 in the lung of diabeticpatients and highlights the changes in clinical outcomes of COVID-19 in normoglycemic and hyperglycemic conditions.
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