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.
Highlights
COVID-19 ScenarioCurrently, there are more than 38 million infected cases and more than 1,000,000 deaths confirmed worldwide due to the spread of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the pathological agent of coronavirus disease 2019 (COVID-19) (WHO, 2020)
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
We have focused on discussing the pathophysiological principles on infection and SARS-CoV2 immune response of lung cells in normoglycemic and hyperglycemic conditions, and assessment findings to frame lung interactions between SARS-CoV-2 infection and diabetes mellitus (DM), paving the way to better understand the unique characteristics of the SARSCoV-2 infection in diabetic lungs
Summary
(1) The airway surface liquid (ASL) plays a pivotal role in lung defense. Diabetes is related with higher ASL glucose concentration, ASL volume accumulation in alveolar space, imbalance of reactive oxidative species (ROS), and inflammatory chemokine production. (2) The COVID-19 infection promotes injuries in type I and type II pneumocytes and lung endothelial lesions, with subsequent additional secretion of protein-rich exudate in the alveolar space and intravascular coagulation in lung vessel, which leads to a reduction in surfactant and gas exchange. (3) The association between diabetes and SARS-CoV-2 increases the glucose and protein concentration in ASL, leading to increase the risk of pneumonia. SARS-CoV-2 in Lung of Diabetics (4) The prevalence and severity of hypoxemia and severe hyperinflammation is higher in COVID-19 diabetic patients. (5) The harmful clinical outcomes and mortality rate of COVID-19 are higher in diabetic subjects
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