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Circadian desynchronization not only disrupts rhythms but also reduces the expression levels of clock and metabolic genes in the heart of C57BL/6J mice with PE-induced cardiomyopathy.

By Akira Kohsaka (229447), Partha Das (659095), Izumi Hashimoto (659096), Tomomi Nakao (659097), Yoko Deguchi (659098), Sabine S. Gouraud (229461), Hidefumi Waki (229450), Yasuteru Muragaki (659099) and Masanobu Maeda (229465)


<p>(A-C) Relative expression levels of genes regulating (A) clock machinery as well as (B) glucose and (C) lipid metabolism in heart. All heart tissues used were from PE-infused animals subjected to either a fixed or a disrupted LD cycle as described in <a href="" target="_blank">Figure 5A</a> (n = 4 per group per time point). To provide a 24-h overall mean expression level, the data over a 24-h time period in each group were also averaged and are expressed using a bar graph format. Data are the mean ± SEM. *<i>P</i><0.05, **<i>P</i><0.01, unpaired two-tailed Student's <i>t</i>-test.</p

Topics: Biological Sciences, Mice Cardiac function, acid oxidative pathway, mitochondrial function, Mitochondrial Respiration, C 57BL mice, mitochondrial metabolism, circadian clock gene Bmal 1 results, gene expression, tricarboxylic acid cycle, mitochondrial oxidative metabolism, mitochondrial defects, Bmal 1 function show, circadian rhythmicity, Regulating Mitochondrial Metabolism, Heart failure, oxidative energy, Circadian Clock Maintains Cardiac Function, circadian clock system
Year: 2014
DOI identifier: 10.1371/journal.pone.0112811.g006
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Provided by: FigShare
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