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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Cardiovascular disease &#40;CVD&#41;&#44; the leading cause of premature death worldwide&#44; including in Europe&#44;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">1</span></a> is predominantly caused by atherosclerosis&#44; a multifactorial disease strongly associated with dyslipidemia&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">2</span></a> Management of dyslipidemia with statins has resulted in decreases in cardiovascular events and mortality&#46; Unfortunately&#44; although aggressive statin therapy leads to significant reductions in total and low-density lipoprotein &#40;LDL&#41; cholesterol&#44; a proportion of treated patients remain at increased risk for cardiovascular mortality&#44; a phenomenon known as residual cardiovascular risk&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">3</span></a> It thus appears that the benefits of statin therapy have reached a plateau&#46; In addition&#44; many patients are unable to tolerate statins due to adverse effects&#44; particularly muscle-related complications &#40;myalgia&#44; myopathy and rhabdomyolysis&#41; and hepatotoxicity&#44; particularly when under intensive therapy&#46;<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">4</span></a> Considering the current unmet needs in the treatment of dyslipidemia&#44; there is considerable potential to reduce CVD mortality and morbidity&#44; which highlights the need for new and effective drugs that can target mediators of atherosclerosis other than cholesterol and lipoproteins&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">Oxidative stress is a crucial factor in the development and progression of atherosclerosis&#44; as it is involved in various molecular mechanisms that contribute to vascular damage and foam cell formation&#46;<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">5</span></a> Oxidative damage to the endothelium and oxidative modification of LDL contribute significantly to atherogenesis&#59; oxidized LDL activates the endothelium via the production of adhesion molecules&#44; recruiting monocytes and T cells&#44; and thus stimulating immune and inflammatory responses&#46;<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">6</span></a> Oxidative stress also appears to be among the multifactorial pathophysiological mechanisms contributing to left ventricular hypertrophy &#40;LVH&#41;&#44;<a class="elsevierStyleCrossRefs" href="#bib0120"><span class="elsevierStyleSup">7&#44;8</span></a> which can be generally viewed as a maladaptive response to chronic pressure overload&#44; and is a major risk factor for atrial fibrillation&#44; diastolic heart failure&#44; systolic heart failure and sudden death in patients with CVD and hypertension&#46;<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">9</span></a> Despite the unequivocal role of oxidative stress mechanisms in the progression of CVD&#44; the impact of therapeutic strategies based on antioxidant diets and compounds on cardiovascular risk and events is controversial&#46;<a class="elsevierStyleCrossRefs" href="#bib0135"><span class="elsevierStyleSup">10&#8211;13</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">The experimental study by Gon&#231;alves et al&#46;<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">14</span></a> in this issue of the <span class="elsevierStyleItalic">Journal</span> assessed the impact of the nitroxide Tempol &#40;4-hydroxy-2&#44;2&#44;6&#44;6-tetramethylpiperidine 1-oxyl&#41;&#44; a superoxide dismutase &#40;SOD&#41; mimetic&#44; on lipid profile and cardiac morphology in the LDL receptor gene knockout &#40;LDLr-&#47;-&#41; mice&#46; After 30 days of a high-fat diet&#44; the animals presented dyslipidemia&#44; with increased concentrations of triglycerides and LDL and very-low density lipoprotein cholesterol&#44; as well as LVH&#46; Tempol &#40;30<span class="elsevierStyleHsp" style=""></span>mg&#47;kg&#41; prevented the development of dyslipidemia and attenuated LVH&#46; The authors claim that Tempol exerted antioxidant effects&#44; thus reducing cardiac oxidative stress&#44; and prevented LVH by alleviating oxidative stress-mediated fibrosis&#46; They also cited previous studies by other groups<a class="elsevierStyleCrossRefs" href="#bib0160"><span class="elsevierStyleSup">15&#8211;17</span></a> suggesting that the beneficial effects of Tempol on dyslipidemia and cardiac damage may be exerted by multiple mechanisms&#44; in pleiotropic-like actions that may explain the restoration of nitric oxide &#40;NO&#41; synthase &#40;NOS&#41; activity and levels of NO&#44; which is recognized as an anti-hypertrophic mediator&#44; as schematized in <a class="elsevierStyleCrossRef" href="#fig0005">Figure 1</a>&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">However&#44; the study by Gon&#231;alves et al&#46;<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">14</span></a> did not present sufficient evidence to confirm this hypothesis&#46; It is also important to assess markers of oxidative stress &#40;such as superoxide anion and peroxynitrite&#41;&#44; measures of antioxidant mechanisms &#40;including SOD activity&#41; and NO pathway markers &#40;such as NOS activity and&#47;or NO levels&#41;&#44; as well as other molecules&#44; particularly oxidized LDL&#46; Furthermore&#44; determining the impact of Tempol on markers of cardiac oxidative stress and fibrosis&#44; as well as on immune and inflammatory response mediators&#44; will be critical for verifying the suggestion that pleiotropic activity could be responsible for its anti-dyslipidemic and anti-fibrotic cardioprotective action&#46; This question is unanswered by the article&#44; although the effects reported for Tempol and simvastatin &#40;20<span class="elsevierStyleHsp" style=""></span>mg&#47;kg&#41; were similar&#46; Statins exert pleiotropic effects in addition to their cholesterol-lowering properties&#44; but these effects mostly require the use of higher doses&#44; which cannot be confirmed by the present study&#46; Overall&#44; the approach of Gon&#231;alves et al&#46; is an interesting one&#44; targeting oxidative stress to improve dyslipidemia and LVH&#44; but the molecular mechanisms involved need further confirmation in preclinical models before being transposed into clinical practice&#44; in which similar interventions targeting oxidative stress have yet to achieve the expected outcomes in terms of reducing cardiovascular risk and mortality&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0025" class="elsevierStylePara elsevierViewall">The author has no conflicts of interest to declare&#46;</p></span></span>"
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          "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Proposed mechanisms to explain the improvement of dyslipidemia and left ventricular hypertrophy by Tempol&#44; a superoxide dismutase mimetic&#44; in agreement with Gon&#231;alves et al&#46;<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">14</span></a> NO&#58; nitric oxide&#59; NOS&#58; nitric oxide synthase&#59; ROS&#58; reactive oxygen species&#59; SOD&#58; superoxide dismutase&#46;</p>"
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Editorial comment
Therapeutic strategies targeting oxidative stress to improve dyslipidemia and left ventricular hypertrophy
Estratégias terapêuticas dirigidas ao stress oxidativo para melhoria da dislipidemia e da hipertrofia ventricular esquerda
Flávio Reisa,b
a Laboratory of Pharmacology & Experimental Therapeutics, Institute for Biomedical Imaging and Life Sciences (IBILI), Faculty of Medicine, University of Coimbra, Coimbra, Portugal
b Centre for Neuroscience and Cell Biology – Institute for Biomedical Imaging and Life Sciences (CNC.IBILI) Research Consortium, University of Coimbra, Coimbra, Portugal
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    "titulo" => "Therapeutic strategies targeting oxidative stress to improve dyslipidemia and left ventricular hypertrophy"
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          "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Proposed mechanisms to explain the improvement of dyslipidemia and left ventricular hypertrophy by Tempol&#44; a superoxide dismutase mimetic&#44; in agreement with Gon&#231;alves et al&#46;<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">14</span></a> NO&#58; nitric oxide&#59; NOS&#58; nitric oxide synthase&#59; ROS&#58; reactive oxygen species&#59; SOD&#58; superoxide dismutase&#46;</p>"
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Cardiovascular disease &#40;CVD&#41;&#44; the leading cause of premature death worldwide&#44; including in Europe&#44;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">1</span></a> is predominantly caused by atherosclerosis&#44; a multifactorial disease strongly associated with dyslipidemia&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">2</span></a> Management of dyslipidemia with statins has resulted in decreases in cardiovascular events and mortality&#46; Unfortunately&#44; although aggressive statin therapy leads to significant reductions in total and low-density lipoprotein &#40;LDL&#41; cholesterol&#44; a proportion of treated patients remain at increased risk for cardiovascular mortality&#44; a phenomenon known as residual cardiovascular risk&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">3</span></a> It thus appears that the benefits of statin therapy have reached a plateau&#46; In addition&#44; many patients are unable to tolerate statins due to adverse effects&#44; particularly muscle-related complications &#40;myalgia&#44; myopathy and rhabdomyolysis&#41; and hepatotoxicity&#44; particularly when under intensive therapy&#46;<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">4</span></a> Considering the current unmet needs in the treatment of dyslipidemia&#44; there is considerable potential to reduce CVD mortality and morbidity&#44; which highlights the need for new and effective drugs that can target mediators of atherosclerosis other than cholesterol and lipoproteins&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">Oxidative stress is a crucial factor in the development and progression of atherosclerosis&#44; as it is involved in various molecular mechanisms that contribute to vascular damage and foam cell formation&#46;<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">5</span></a> Oxidative damage to the endothelium and oxidative modification of LDL contribute significantly to atherogenesis&#59; oxidized LDL activates the endothelium via the production of adhesion molecules&#44; recruiting monocytes and T cells&#44; and thus stimulating immune and inflammatory responses&#46;<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">6</span></a> Oxidative stress also appears to be among the multifactorial pathophysiological mechanisms contributing to left ventricular hypertrophy &#40;LVH&#41;&#44;<a class="elsevierStyleCrossRefs" href="#bib0120"><span class="elsevierStyleSup">7&#44;8</span></a> which can be generally viewed as a maladaptive response to chronic pressure overload&#44; and is a major risk factor for atrial fibrillation&#44; diastolic heart failure&#44; systolic heart failure and sudden death in patients with CVD and hypertension&#46;<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">9</span></a> Despite the unequivocal role of oxidative stress mechanisms in the progression of CVD&#44; the impact of therapeutic strategies based on antioxidant diets and compounds on cardiovascular risk and events is controversial&#46;<a class="elsevierStyleCrossRefs" href="#bib0135"><span class="elsevierStyleSup">10&#8211;13</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">The experimental study by Gon&#231;alves et al&#46;<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">14</span></a> in this issue of the <span class="elsevierStyleItalic">Journal</span> assessed the impact of the nitroxide Tempol &#40;4-hydroxy-2&#44;2&#44;6&#44;6-tetramethylpiperidine 1-oxyl&#41;&#44; a superoxide dismutase &#40;SOD&#41; mimetic&#44; on lipid profile and cardiac morphology in the LDL receptor gene knockout &#40;LDLr-&#47;-&#41; mice&#46; After 30 days of a high-fat diet&#44; the animals presented dyslipidemia&#44; with increased concentrations of triglycerides and LDL and very-low density lipoprotein cholesterol&#44; as well as LVH&#46; Tempol &#40;30<span class="elsevierStyleHsp" style=""></span>mg&#47;kg&#41; prevented the development of dyslipidemia and attenuated LVH&#46; The authors claim that Tempol exerted antioxidant effects&#44; thus reducing cardiac oxidative stress&#44; and prevented LVH by alleviating oxidative stress-mediated fibrosis&#46; They also cited previous studies by other groups<a class="elsevierStyleCrossRefs" href="#bib0160"><span class="elsevierStyleSup">15&#8211;17</span></a> suggesting that the beneficial effects of Tempol on dyslipidemia and cardiac damage may be exerted by multiple mechanisms&#44; in pleiotropic-like actions that may explain the restoration of nitric oxide &#40;NO&#41; synthase &#40;NOS&#41; activity and levels of NO&#44; which is recognized as an anti-hypertrophic mediator&#44; as schematized in <a class="elsevierStyleCrossRef" href="#fig0005">Figure 1</a>&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">However&#44; the study by Gon&#231;alves et al&#46;<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">14</span></a> did not present sufficient evidence to confirm this hypothesis&#46; It is also important to assess markers of oxidative stress &#40;such as superoxide anion and peroxynitrite&#41;&#44; measures of antioxidant mechanisms &#40;including SOD activity&#41; and NO pathway markers &#40;such as NOS activity and&#47;or NO levels&#41;&#44; as well as other molecules&#44; particularly oxidized LDL&#46; Furthermore&#44; determining the impact of Tempol on markers of cardiac oxidative stress and fibrosis&#44; as well as on immune and inflammatory response mediators&#44; will be critical for verifying the suggestion that pleiotropic activity could be responsible for its anti-dyslipidemic and anti-fibrotic cardioprotective action&#46; This question is unanswered by the article&#44; although the effects reported for Tempol and simvastatin &#40;20<span class="elsevierStyleHsp" style=""></span>mg&#47;kg&#41; were similar&#46; Statins exert pleiotropic effects in addition to their cholesterol-lowering properties&#44; but these effects mostly require the use of higher doses&#44; which cannot be confirmed by the present study&#46; Overall&#44; the approach of Gon&#231;alves et al&#46; is an interesting one&#44; targeting oxidative stress to improve dyslipidemia and LVH&#44; but the molecular mechanisms involved need further confirmation in preclinical models before being transposed into clinical practice&#44; in which similar interventions targeting oxidative stress have yet to achieve the expected outcomes in terms of reducing cardiovascular risk and mortality&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0025" class="elsevierStylePara elsevierViewall">The author has no conflicts of interest to declare&#46;</p></span></span>"
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ISSN: 21742049
Original language: English
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Revista Portuguesa de Cardiologia (English edition)
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