Lipid and Mitochondrial Energetic Metabolism: Interconnected Pathways in Human Health and Disease

Call for Papers

Mitochondria have a central position in global energy production by generating a significant amount of ATP during glucose and fat oxidation. An increased energetic need is met by enhancing mitochondrial mass and inducing the expression of oxidative phosphorylation genes. Conversely, nutrient overload shifts systemic metabolism towards a state of heightened lipogenesis in liver and increased lipid storage in peripheral, insulin-sensitive tissues. The molecular pathways that orchestrate the adaptation to energetic imbalance are finely regulated and respond to specific nutrient signals (AMP/ATP, NAD+/NADH, and reactive oxygen species (ROS)), which in turn modulate key molecular factors including AMPK, SIRT1, and the family of PGC-1 transcriptional coactivators that are ultimately involved in the regulation of the expression of both mitochondrial and lipid metabolic genes.

In mammalian systems saturated fat constitutes a large bulk of circulating fatty acids together with unsaturated fatty acids mainly derived from diet. Polyunsatured fatty acids (PUFAs) can readily be oxidized by ROS and reactive nitrogen species (RNS) and generate very high reactive species capable of several biological activities both beneficial and harmful particularly in mitochondria. A tight regulation of lipid and mitochondrial metabolism is necessary and pivotal for avoiding the mitochondrial dysfunctions and altered lipid homeostasis typical of a variety of pathological states including canonical metabolic diseases (e.g., type 2 diabetes mellitus, cardiovascular diseases, and obesity), cancer, and neurodegeneration. Therefore, the comprehension of the mechanisms governing metabolic homeostasis is a timely and emerging research topic that will have central implications in the understanding of numerous disease states.

We encourage authors to submit original research as well as review articles that will improve our knowledge on the molecular events underlying the regulation of lipid and mitochondrial metabolism and its implication in the aetiology and progression of human pathological conditions. Potential topics include, but are not limited to:

• Emerging metabolic routes regulating lipid catabolism (e.g., lipophagy)
• Signalling pathways regulating the cross-talk between mitochondrial and lipid metabolism
• Oxidized lipids as novel signaling intermediates
• Dietary lipids and mitochondrial phospholipid interaction
• ROS/RNS and lipid cross-talk in mitochondrial metabolism and turnover
• Mitochondrial and lipid dysmetabolism in human diseases

Before submission authors should carefully read over the journal’s Author Guidelines, which are located at http://www.hindawi.com/journals/ijcb/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/submit/journals/ijcb/limit/ according to the following timetable:

Lead Guest Editor

• Katia Aquilano, Department of Biology, University of Rome “Tor Vergata,” Rome, Italy

Guest Editors

• Maria Rosa Ciriolo, Department of Biology, University of Rome “Tor Vergata,” Rome, Italy
• Julie St-Pierre, Department of Biochemistry, McGill University, Montreal, QC, Canada
• Ethan J. Anderson, Department of Pharmacology and Toxicology, Brody School of Medicine, East Carolina University, Greenville, NC, USA