Growth Factor Signalling, Cellular Energy Metabolism and Obesity
A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".
Deadline for manuscript submissions: closed (31 March 2022) | Viewed by 472
Special Issue Editor
Interests: energy metabolism; NAD (nicotinamide adenine dinucleotide) metabolism; growth factor signaling; adipose tissue biology
Special Issue Information
Dear Colleagues,
Growth factor signalling pathways are part of a complex network responsible for maintaining whole body metabolic homeostasis. Together with factors sensing nutrient and cellular energy status, feeding regulatory centers in the central nervous system (CNS) and hormonal signals from metabolic tissues, they tightly regulate cellular energy balance by impacting the intake, storage and utilisation of nutrients.
The insulin/insulin-like growth factor (IGF) signaling pathway is a major signaling pathway that regulates cellular growth and survival. Insulin and IGF-I signal through a complex system of homo- and heterodimeric receptors and binding proteins to activate the phosphoinositid-3-kinase (PI3K)/AKT/mechanistic target of rapamycin (mTOR) pathway. mTOR complex 1 is a nutrient sensing kinase which balances cellular growth with autophagy. There is reciprocal regulation between the mTOR and another energy sensing network, the AMP-activated kinase (AMPK)—Sirtuin 1 axis, which is activated by a low cellular energy status, which negatively regulates mTORC1 activity.
In this Special Issue, we will take a closer look at the insulin/IGF-I signaling cascade, its cross-talk with AMPK and Sirtuin1 signaling pathways, pathogenetic changes of this network in obesity, and their impact on cellular energy metabolism in metabolic tissues.
Dr. Antje Garten
Guest Editor
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Keywords
- insulin
- NAD
- mTOR
- nutrient sensing
- AMPK
- Sirtuin1
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