Negative regulation of PGC-1α by NF-κB
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Date
2014-01-10
Authors
Blant, Alexandra
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Abstract
The normal adult heart prefers fatty acids as an energy substrate. In the case of heart
failure, the heart switches its preference from fatty acids to glucose, adopting a pattern
similar to fetal metabolism. PGC-1α is heavily involved in the shift towards glucose oxidation. p65, which belongs to the NF-κB transcription factor family is another crucial molecule involved in maintaining cardiac homeostasis. There is a substantial amount of evidence suggesting that PGC-1α and NF-κB directly interact,
thereby connecting metabolic and inflammatory processes. Dysregulation of
either PGC-1α or NF-κB signalling correlates to many diseases including heart disease.
In this study, we provide further evidence that the NF-κB family has the ability to repress
PGC-1α. We also show that the PGC-1α promoter contains a p65 binding site through
which p65 imparts control on the PGC-1α gene. Metabolic homeostasis and inflammation
pathways are closely linked and play crucial roles in heart dysfunction.
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Keywords
heart disease, PGC-1α promoter, NF-κB, inflammation, fatty acid metabolism, metabolism and inflammation, fetal metabolic profile, cardiac homeostasis