2007
DOI: 10.1253/circj.71.1893
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Transient Enhancement of Oxidant Stress and Collagen Turnover in Patients With Acute Worsening of Congestive Heart Failure

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Cited by 14 publications
(5 citation statements)
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“…Free-radical generation by the failing myocardium has been proposed as linked to myocardial remodeling [32] and was shown to induce Akt activation by oxidizing phosphatase and tensin homolog deleted from chromosome 10 (PTEN) [33], providing a defensive mechanism against the deleterious effects of the free radicals. Our findings that Akt was activated in the ISO group were in agreement with this widely accepted notion.…”
Section: Discussionmentioning
confidence: 99%
“…Free-radical generation by the failing myocardium has been proposed as linked to myocardial remodeling [32] and was shown to induce Akt activation by oxidizing phosphatase and tensin homolog deleted from chromosome 10 (PTEN) [33], providing a defensive mechanism against the deleterious effects of the free radicals. Our findings that Akt was activated in the ISO group were in agreement with this widely accepted notion.…”
Section: Discussionmentioning
confidence: 99%
“…For anabolic BTMs, bone ALP is not renally cleared and may have utility in the setting of renal insufficiency (34 ). Most BTMs are present in type I collagen in nonskeletal tissues, therefore disease processes involving matrix remodeling in other tissues, such as systemic sclerosis, congestive heart failure, or dilated cardiomyopathy have been shown to increase BTM concentrations (35–37 ).…”
Section: Preanalytic Factors In the Measurement Of Btmsmentioning
confidence: 99%
“…While in vivo animal models of cardiac pathology have highlighted redox-balance as a mediator of heart failure progression the translation of this to a clinical setting is becoming more apparent. Congestive heart failure progression, dilated, and ischemic cardiomyopathy, end stage heart failure, chronic heart failure, and ethanol induced cardiac abnormalities are all associated with a concurrent rise in free radical generation (Jaatinen et al, 1993 ; Landmesser, 2002 ; Maack et al, 2003 ; Giordano, 2005 ; Kunishige et al, 2007 ; Nakamura et al, 2015 ; Shah, 2015 ). Additionally, it is emerging that the enzymes and cellular sources driving increased ROS production may be divergent depending on the pathology involved such as systolic vs. diastolic dysfunction (Münzel et al, 2015 ).…”
Section: Ros-sources and Functionmentioning
confidence: 99%
“…Heart failure is associated with a shift in the redox environment of the heart to a pro-oxidative state. Although, there is evidence for a reduction in the antioxidant capacity of the heart during disease, the principal driving force toward this pro-oxidative milieu appears to be excessive ROS production (Landmesser, 2002 ; Maack et al, 2003 ; Giordano, 2005 ; Kunishige et al, 2007 ; Nakamura et al, 2015 ). To investigate the physiological consequence of this on the contractile ability of the myocardium, cardiomyocytes have been exposed to various forms of ROS, had oxidant formation inhibited or applied with exogenous anti-oxidants.…”
Section: Excitation Contraction Couplingmentioning
confidence: 99%