We are analyzing https://link.springer.com/article/10.1007/s11010-011-0711-y.

Title:
Temporal relation of cardiac hypertrophy, oxidative stress, and fatty acid metabolism in spontaneously hypertensive rat | Molecular and Cellular Biochemistry
Description:
Left ventricular hypertrophy is an adaptive response to hypertension, and an independent clinical risk factor for cardiac failure, sudden death, and myocardial infarction. As regression of cardiac hypertrophy is associated with a lower likelihood of cardiovascular events, it is recognized as a target of antihypertensive therapy. This necessitates identification of factors associated with the initiation and progression of hypertrophy. Oxidative stress and metabolic shift are intimately linked with myocardial hypertrophy, but their interrelationship is not clearly understood. This study proposes to identify the temporal sequence of events so as to distinguish whether oxidative stress and metabolic shift are a cause or consequence of hypertrophy. Spontaneously hypertensive rat (SHR) was used as the experimental model. Cardiac hypertrophy was apparent at 2 months of age, as assessed by hypertrophy index and brain natriuretic peptide gene expression. Enhanced myocardial lipid peroxidation accompanied by nuclear factor-kappa B gene expression in one-month-old SHR suggests that oxidative stress precedes the development of hypertrophy. Metabolic shift identified by reduction in the expression of peroxisome proliferator-activated receptor-alpha, medium chain acyl CoA dehydrogenase, and carnitine palmitoyltransferase 1β was seen at 4 months of age, implying that reduction of fatty acid oxidation is a consequence of hypertrophy. Information on the temporal sequence of events associated with hypertrophy will help in the prevention and reversal of cardiac remodeling. Investigations aimed at prevention of hypertrophy should address reduction of oxidative stress. Both, oxidative stress and metabolic modulation have to be considered for studies that focus on the regression of hypertrophy.
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article, hypertrophy, google, scholar, pubmed, cardiac, cas, oxidative, stress, spontaneously, hypertensive, metabolism, metabolic, research, fatty, acid, nair, hypertension, rats, cell, india, privacy, cookies, content, analysis, publish, january, myocardial, expression, access, med, mol, technology, data, information, search, temporal, rat, purushothaman, renuka, regression, shift, gene, cardiol, biochem, heart, physiol, institute, medical, log,

Topics {✒️}

peroxisome proliferator-activated receptor-alpha nuclear factor-κb–dependent induction month download article/chapter fatty acid metabolism real-time quantitative pcr ace/ache/buche inhibitors delta delta ct–method normotensive wistar-kyoto rats nf-κb induces regression metabolic shift identified fatty acid oxidation full article pdf spontaneously hypertensive rats related subjects chronic pressure overload privacy choices/manage cookies spontaneously hypertensive rat villa-abrille mc metabolic shift rubber research institute nuclear factor-kappa cellular biochemistry aims microsomal lipid peroxidation financial support extended tumor necrosis factor lipoprotein metabolism interleukin-8 gene expression laboratory animal science seymour a-ml strain-stimulated hypertrophy european economic area oxidative stress precedes carnitine palmitoyltransferase 1β increased oxidative stress decreases oxidative stress serum malondialdehyde level failing human heart adenine nucleotide translocator-1 blood pressure control article molecular article purushothaman conditions privacy policy check access instant access accepting optional cookies med clin north article log metabolic abnormalities spontaneously hypertensive metabolic modulation

Questions {❓}

Grossman E (2008) Does increased oxidative stress cause hypertension?
Álvarez MC, Caldiz C, Fantinelli JC et al (2008) Is cardiac hypertrophy in spontaneously hypertensive rats the cause or the consequence of oxidative stress?

Schema {🗺️}

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         description:Left ventricular hypertrophy is an adaptive response to hypertension, and an independent clinical risk factor for cardiac failure, sudden death, and myocardial infarction. As regression of cardiac hypertrophy is associated with a lower likelihood of cardiovascular events, it is recognized as a target of antihypertensive therapy. This necessitates identification of factors associated with the initiation and progression of hypertrophy. Oxidative stress and metabolic shift are intimately linked with myocardial hypertrophy, but their interrelationship is not clearly understood. This study proposes to identify the temporal sequence of events so as to distinguish whether oxidative stress and metabolic shift are a cause or consequence of hypertrophy. Spontaneously hypertensive rat (SHR) was used as the experimental model. Cardiac hypertrophy was apparent at 2 months of age, as assessed by hypertrophy index and brain natriuretic peptide gene expression. Enhanced myocardial lipid peroxidation accompanied by nuclear factor-kappa B gene expression in one-month-old SHR suggests that oxidative stress precedes the development of hypertrophy. Metabolic shift identified by reduction in the expression of peroxisome proliferator-activated receptor-alpha, medium chain acyl CoA dehydrogenase, and carnitine palmitoyltransferase 1β was seen at 4 months of age, implying that reduction of fatty acid oxidation is a consequence of hypertrophy. Information on the temporal sequence of events associated with hypertrophy will help in the prevention and reversal of cardiac remodeling. Investigations aimed at prevention of hypertrophy should address reduction of oxidative stress. Both, oxidative stress and metabolic modulation have to be considered for studies that focus on the regression of hypertrophy.
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