Abstract
Reactive oxygen species (ROS) plays a role in intracellular signal transduction under physiological conditions while also playing an essential role in diseases such as hypertension, ischemic heart disease, and diabetes, as well as in the process of aging. The influence of ROS has some influence on the frequent occurrence of cardiovascular diseases (CVD) in diabetic patients. In this review, we considered the pathophysiological relationship between diabetes and CVD from the perspective of ROS. In addition, considering organ damage due to ROS elevation during ischemia–reperfusion, we discussed heart and lung injuries. Furthermore, we have focused on the transient receptor potential (TRP) channels and L-type calcium channels as molecular targets for ROS in ROS-induced tissue damages and have discussed about the pathophysiological mechanism of the injury.
Highlights
At first glance, diabetes, which causes abnormal blood glucose control, and ischemia–reperfusion injury (IRI) of the heart, which causes myocardial infarction, seem to have nothing in common
Oxidative stress is based on the balance between oxidant and antioxidant activities derived from numerous molecules and pathways
A common mechanism is involved in the pathology of diabetes and IRI
Summary
Diabetes, which causes abnormal blood glucose control, and ischemia–reperfusion injury (IRI) of the heart, which causes myocardial infarction, seem to have nothing in common. When ATP production in hypoxia is insufficient, cardiomyocytes activates the KATP channels [174] and cause cell hyperpolarization, thereby preventing arrhythmia This process may be affected by electrical disturbances induced by TRPM4 protein, because the channel is sensitive to Ca2+ and ATP [175, 176]. An indirect evidence of this finding is that ET-1 could increase the production of ROS in PASMCs [230,231,232] This hypothesis has not been tested in pulmonary circulation, but the activation of L-type VGCC induced by ET-1 in isolated cardiomyocytes is known to be mediated by.O−2 [233]
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