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Cross-Talk of NADPH Oxidases and Inflammation in Obesity. | LitMetric

Cross-Talk of NADPH Oxidases and Inflammation in Obesity.

Antioxidants (Basel)

Department of Medicine III, University Hospital and Faculty of Medicine Carl Gustav Carus, TUD Dresden University of Technology, Fetscherstraße 74, 01307 Dresden, Germany.

Published: August 2023

AI Article Synopsis

  • * NADPH oxidases produce reactive oxygen species that contribute to these health issues, impairing the body's ability to fight inflammation and oxidative damage.
  • * Recent evidence links COVID-19 to increased oxidative stress and inflammation, suggesting a higher risk of severe complications related to cardiometabolic diseases post-infection.

Article Abstract

Obesity is a major risk factor for cardiovascular and metabolic diseases. Multiple experimental and clinical studies have shown increased oxidative stress and inflammation linked to obesity. NADPH oxidases are major sources of reactive oxygen species in the cardiovascular system and in metabolically active cells and organs. An impaired balance due to the increased formation of reactive oxygen species and a reduced antioxidative capacity contributes to the pathophysiology of cardiovascular and metabolic diseases and is linked to inflammation as a major pathomechanism in cardiometabolic diseases. Non-alcoholic fatty liver disease is particularly characterized by increased oxidative stress and inflammation. In recent years, COVID-19 infections have also increased oxidative stress and inflammation in infected cells and tissues. Increasing evidence supports the idea of an increased risk for severe clinical complications of cardiometabolic diseases after COVID-19. In this review, we discuss the role of oxidative stress and inflammation in experimental models and clinical studies of obesity, cardiovascular diseases, COVID-19 infections and potential therapeutic strategies.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10451527PMC
http://dx.doi.org/10.3390/antiox12081589DOI Listing

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