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.
Identifer | oai:union.ndltd.org:LACETR/oai:collectionscanada.gc.ca:MWU.1993/23146 |
Date | 10 January 2014 |
Creators | Blant, Alexandra |
Contributors | Czubryt, Michael (Physiology), Duhamel, Todd (Kinesiology and Recreation Management) Singal, Pawan (Physiology) Kirshenbaum, Lorrie (Physiology) |
Source Sets | Library and Archives Canada ETDs Repository / Centre d'archives des thèses électroniques de Bibliothèque et Archives Canada |
Detected Language | English |
Page generated in 0.0016 seconds