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Regulation of oxidative stress and cardioprotection in diabetes mellitus.

Hayashi T, Mori T, Yamashita C, Miyamura M - Curr Cardiol Rev (2008)

Bottom Line: On the other hand, the renin-angiotensin system is activated in diabetes, and local angiotensin II production may lead to oxidative damage via the angiotensin II type 1 receptor.Basic and clinical data indicate that angiotensin II receptor blockers have the potential to preserve left ventricular function and prevent cardiac remodeling that is exaggerated by oxidative stress in patients with diabetes.Thus, alleviation of oxidative stress might be one possible strategy in the treatment of diabetic patients associated with sleep apnea.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine III, Osaka Medical College.

ABSTRACT
Analysis of the Framingham data has shown that the risk of heart failure is increased substantially among diabetic patients, while persons with the metabolic syndrome have an increased risk of both atherosclerosis and diabetes mellitus. Sleep apnea may be related to the metabolic syndrome and systemic inflammation through hypoxia, which might also cause the cardiac remodeling by increased oxidative stress. On the other hand, the renin-angiotensin system is activated in diabetes, and local angiotensin II production may lead to oxidative damage via the angiotensin II type 1 receptor. Basic and clinical data indicate that angiotensin II receptor blockers have the potential to preserve left ventricular function and prevent cardiac remodeling that is exaggerated by oxidative stress in patients with diabetes. Thus, alleviation of oxidative stress might be one possible strategy in the treatment of diabetic patients associated with sleep apnea.

No MeSH data available.


Related in: MedlinePlus

Role of oxidative stress in the progression of cardiovascular diseases accompanied by diabetes mellitus. Diabetes mellitus induced oxidative stress at least partly through NADPH oxidase activation, and consequently accelerated the progression of cardiovascular diseases. In addition, hypoxia might be implicated in the development of diabetes mellitus and production of reactive oxygen species (ROS), associated with the insult to mitochondria in cardiomyocytes by hypoxia itself.
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Figure 3: Role of oxidative stress in the progression of cardiovascular diseases accompanied by diabetes mellitus. Diabetes mellitus induced oxidative stress at least partly through NADPH oxidase activation, and consequently accelerated the progression of cardiovascular diseases. In addition, hypoxia might be implicated in the development of diabetes mellitus and production of reactive oxygen species (ROS), associated with the insult to mitochondria in cardiomyocytes by hypoxia itself.

Mentions: NADPH oxidase is a major producer of ROS. This enzyme is composed of two membrane-bound subunits (gp91 phox and p22phox), as well as four cytosolic subunits (p40phox, p47phox, p67phox, and rac-1). Both angiotensin II and inflammatory cytokines have already been shown to stimulate NADPH oxidase, while hypoxic stress may be similarly important for its activation. In fact, Zhan et al. [58] reported that NADPH oxidase-derived ROS contribute to oxidative injury in the brains of mice exposed to intermittent hypoxia. Moreover, we have shown that hypoxia increases ROS production by NADPH oxidase in the aorta and LV myocardium, and consequently accelerates both atherosclerosis and LV remodeling [53,54]. Thus, intermittent hypoxia might enhance oxidative stress at least partly through activation of NADPH oxidase. Oxidative stress is also responsible for the activation of NF-κB [59,60], which regulates the expression of inflammatory cytokines and mediates monocyte-endothelial cell adhesion. We observed that hypoxia activates NF-κB in the LV myocardium of atherogenic mice [53]. This raises the possibility that NF-κB is an essential factor for the development of cardiovascular disease associated with hypoxic states. Taken together, these findings suggest that cardiovascular disease might be promoted by oxidative stress related to intermittent hypoxia (Fig. 3). In addition, NADPH oxidase might be a useful target for therapeutic intervention to prevent cardiovascular disease in patients with OSAS.


Regulation of oxidative stress and cardioprotection in diabetes mellitus.

Hayashi T, Mori T, Yamashita C, Miyamura M - Curr Cardiol Rev (2008)

Role of oxidative stress in the progression of cardiovascular diseases accompanied by diabetes mellitus. Diabetes mellitus induced oxidative stress at least partly through NADPH oxidase activation, and consequently accelerated the progression of cardiovascular diseases. In addition, hypoxia might be implicated in the development of diabetes mellitus and production of reactive oxygen species (ROS), associated with the insult to mitochondria in cardiomyocytes by hypoxia itself.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2801856&req=5

Figure 3: Role of oxidative stress in the progression of cardiovascular diseases accompanied by diabetes mellitus. Diabetes mellitus induced oxidative stress at least partly through NADPH oxidase activation, and consequently accelerated the progression of cardiovascular diseases. In addition, hypoxia might be implicated in the development of diabetes mellitus and production of reactive oxygen species (ROS), associated with the insult to mitochondria in cardiomyocytes by hypoxia itself.
Mentions: NADPH oxidase is a major producer of ROS. This enzyme is composed of two membrane-bound subunits (gp91 phox and p22phox), as well as four cytosolic subunits (p40phox, p47phox, p67phox, and rac-1). Both angiotensin II and inflammatory cytokines have already been shown to stimulate NADPH oxidase, while hypoxic stress may be similarly important for its activation. In fact, Zhan et al. [58] reported that NADPH oxidase-derived ROS contribute to oxidative injury in the brains of mice exposed to intermittent hypoxia. Moreover, we have shown that hypoxia increases ROS production by NADPH oxidase in the aorta and LV myocardium, and consequently accelerates both atherosclerosis and LV remodeling [53,54]. Thus, intermittent hypoxia might enhance oxidative stress at least partly through activation of NADPH oxidase. Oxidative stress is also responsible for the activation of NF-κB [59,60], which regulates the expression of inflammatory cytokines and mediates monocyte-endothelial cell adhesion. We observed that hypoxia activates NF-κB in the LV myocardium of atherogenic mice [53]. This raises the possibility that NF-κB is an essential factor for the development of cardiovascular disease associated with hypoxic states. Taken together, these findings suggest that cardiovascular disease might be promoted by oxidative stress related to intermittent hypoxia (Fig. 3). In addition, NADPH oxidase might be a useful target for therapeutic intervention to prevent cardiovascular disease in patients with OSAS.

Bottom Line: On the other hand, the renin-angiotensin system is activated in diabetes, and local angiotensin II production may lead to oxidative damage via the angiotensin II type 1 receptor.Basic and clinical data indicate that angiotensin II receptor blockers have the potential to preserve left ventricular function and prevent cardiac remodeling that is exaggerated by oxidative stress in patients with diabetes.Thus, alleviation of oxidative stress might be one possible strategy in the treatment of diabetic patients associated with sleep apnea.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine III, Osaka Medical College.

ABSTRACT
Analysis of the Framingham data has shown that the risk of heart failure is increased substantially among diabetic patients, while persons with the metabolic syndrome have an increased risk of both atherosclerosis and diabetes mellitus. Sleep apnea may be related to the metabolic syndrome and systemic inflammation through hypoxia, which might also cause the cardiac remodeling by increased oxidative stress. On the other hand, the renin-angiotensin system is activated in diabetes, and local angiotensin II production may lead to oxidative damage via the angiotensin II type 1 receptor. Basic and clinical data indicate that angiotensin II receptor blockers have the potential to preserve left ventricular function and prevent cardiac remodeling that is exaggerated by oxidative stress in patients with diabetes. Thus, alleviation of oxidative stress might be one possible strategy in the treatment of diabetic patients associated with sleep apnea.

No MeSH data available.


Related in: MedlinePlus