Chlamydia pneumoniae and Oxidative Stress in Cardiovascular Disease: State of the Art and Prevention Strategies

International Journal of Molecular Sciences

Marisa Di Pietro²  Simone Filardo²  Fiorenzo De Santis²  Paola Mastromarino²  Rosa Sessa¹ 

[1] Department of Public Health and Infectious Diseases, “Sapienza” University, Rome 00185, Italy;

关键词: C. pneumoniae;    cardiovascular disease;    oxidative stress;    prevention strategies;   

DOI  :  10.3390/ijms16010724

来源: mdpi

【 摘 要 】

Chlamydia pneumoniae, a pathogenic bacteria responsible for respiratory tract infections, is known as the most implicated infectious agent in atherosclerotic cardiovascular diseases (CVDs). Accumulating evidence suggests that C. pneumoniae-induced oxidative stress may play a critical role in the pathogenesis of CVDs. Indeed, the overproduction of reactive oxygen species (ROS) within macrophages, endothelial cells, platelets and vascular smooth muscle cells (VSMCs) after C. pneumoniae exposure, has been shown to cause low density lipoprotein oxidation, foam cell formation, endothelial dysfunction, platelet adhesion and aggregation, and VSMC proliferation and migration, all responsible for the typical pathological changes of atherosclerotic plaque. The aim of this review is to improve our insight into C. pneumoniae-induced oxidative stress in order to suggest potential strategies for CVD prevention. Several antioxidants, acting on multi-enzymatic targets related to ROS production induced by C. pneumoniae, have been discussed. A future strategy for the prevention of C. pneumoniae-associated CVDs will be to target chlamydial HSP60, involved in oxidative stress.

【 授权许可】

CC BY   
© 2014 by the authors; licensee MDPI, Basel, Switzerland.