AI Article Synopsis
- Reactive oxygen species (ROS) contribute to cardiovascular diseases like atherosclerosis and hypertension by acting as intracellular second messengers and triggering unique signaling pathways.
- Angiotensin II (AngII), a strong cardiovascular pathogen, increases ROS production through vascular NADPH oxidases, which then activates important kinases involved in cardiovascular remodeling.
- Recent advances in gene transfer and knockout techniques have aided studies that reveal how ROS signal transduction mechanisms related to AngII promote changes in cardiovascular structure and function.
Article Abstract
Reactive oxygen species (ROS) are proposed to induce cardiovascular diseases, such as atherosclerosis and hypertension, through several mechanisms. One such mechanism involves ROS acting as intracellular second messengers, which lead to induction of unique signal transductions. Angiotensin II (AngII), a potent cardiovascular pathogen, stimulates ROS production through vascular NADPH oxidases. The ROS production induced by AngII activates downstream ROS-sensitive kinases that are critical in mediating cardiovascular remodeling. Recent advances in gene transfer/knockout techniques have lead to numerous in vitro and in vivo studies that identify the potential components and mechanisms of ROS signal transduction by AngII which promote cardiovascular remodeling. In this review, we will focus our discussion on the signal transduction research elucidating ROS production and function induced by AngII using currently available molecular biotechnologies.
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| http://dx.doi.org/10.2174/138920106776597667 | DOI Listing |
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