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.
<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="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0112811#pone-0112811-g005" 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
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
DOI identifier: 10.1371/journal.pone.0112811.g006
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