Biolipids molecules have different and multiple biological activities and functions. Biolipids covers the most basic biolipids (including fatty acids, glycerides, phospholipids, and sphingolipids) as well as lipoproteins and steroids. Several aspects of lipid metabolism, such as biosynthesis, oxidation, uptake, enzymes, regulation, and signalling pathways, have been shown to be essential in the progression of cardiovascular disease. Mitochondria produce ATP through ß oxidation, TCA cycle and mitochondrial electron transport chain, which plays an important role in intracellular energy metabolism. Meanwhile, reactive oxygen species (ROS) produced in these processes frequently promote the occurrence of cardiovascular diseases.
Iron is present in various forms in heme and iron-sulfur (Fe-S) cluster binding proteins and is involved in various enzymatic reactions such as aerobic respiration, TCA cycling, DNA synthesis, and oxygen transport and storage. Ferroptosis is an iron-driven programmed cell death characterized by the excessive lipid peroxidation products and ROS. Ferroptosis has been found in the pathogenesis and development of cardiovascular diseases. Several aspects of lipid metabolism, such as biosynthesis, oxidation, uptake, enzymes, regulation, and signaling pathways, have been shown to be essential in the progression of cardiovascular disease. The recent finding of altered lipid metabolism accompanying ferroptosis provides interesting insights into the interaction between iron death and lipid metabolism. ACSL4, for instance, induces ferroptosis through accumulation of phospholipids in oxidized cell membranes. The processes of lipid synthesis, storage and degradation are associated with ferroptosis. Lipid metabolism regulates ferroptosis via several pathways and determines cell sensitivity to ferroptosis. Both lipid and iron metabolism can affect ferroptosis and their pathways are closely related. Therefore, it's vital to review the role of supermolecule metabolism and ferroptosis in cardiovascular diseases and their crosstalk.
The research topic aims to gather and publish a series of recent research articles on the role of lipid metabolism and/or ferroptosis in cardiovascular disease, highlight major findings and up to date advances in this field. This will open up research directions, enrich research contents and explore deeper molecular and cellular mechanisms in the cardiac metabolism research field.
We will welcome the submission of Original Research articles and state-of-the-art Reviews, but also Mini Reviews, Brief Research Reports, Hypotheses articles and Opinion articles that focus on but are not limited to the following:
- Polyunsaturated fatty acids and iron death
- Lipid and/or iron metabolism
- Lipid metabolism and mitochondria
- Crosstalk between mitochondrial respiratory function, oxidative stress and ferroptosis
- Iron metabolism and lipid peroxidation
- Lipid metabolism and NAD(P)H
- Therapeutics targeting lipid metabolism and iron death
Biolipids molecules have different and multiple biological activities and functions. Biolipids covers the most basic biolipids (including fatty acids, glycerides, phospholipids, and sphingolipids) as well as lipoproteins and steroids. Several aspects of lipid metabolism, such as biosynthesis, oxidation, uptake, enzymes, regulation, and signalling pathways, have been shown to be essential in the progression of cardiovascular disease. Mitochondria produce ATP through ß oxidation, TCA cycle and mitochondrial electron transport chain, which plays an important role in intracellular energy metabolism. Meanwhile, reactive oxygen species (ROS) produced in these processes frequently promote the occurrence of cardiovascular diseases.
Iron is present in various forms in heme and iron-sulfur (Fe-S) cluster binding proteins and is involved in various enzymatic reactions such as aerobic respiration, TCA cycling, DNA synthesis, and oxygen transport and storage. Ferroptosis is an iron-driven programmed cell death characterized by the excessive lipid peroxidation products and ROS. Ferroptosis has been found in the pathogenesis and development of cardiovascular diseases. Several aspects of lipid metabolism, such as biosynthesis, oxidation, uptake, enzymes, regulation, and signaling pathways, have been shown to be essential in the progression of cardiovascular disease. The recent finding of altered lipid metabolism accompanying ferroptosis provides interesting insights into the interaction between iron death and lipid metabolism. ACSL4, for instance, induces ferroptosis through accumulation of phospholipids in oxidized cell membranes. The processes of lipid synthesis, storage and degradation are associated with ferroptosis. Lipid metabolism regulates ferroptosis via several pathways and determines cell sensitivity to ferroptosis. Both lipid and iron metabolism can affect ferroptosis and their pathways are closely related. Therefore, it's vital to review the role of supermolecule metabolism and ferroptosis in cardiovascular diseases and their crosstalk.
The research topic aims to gather and publish a series of recent research articles on the role of lipid metabolism and/or ferroptosis in cardiovascular disease, highlight major findings and up to date advances in this field. This will open up research directions, enrich research contents and explore deeper molecular and cellular mechanisms in the cardiac metabolism research field.
We will welcome the submission of Original Research articles and state-of-the-art Reviews, but also Mini Reviews, Brief Research Reports, Hypotheses articles and Opinion articles that focus on but are not limited to the following:
- Polyunsaturated fatty acids and iron death
- Lipid and/or iron metabolism
- Lipid metabolism and mitochondria
- Crosstalk between mitochondrial respiratory function, oxidative stress and ferroptosis
- Iron metabolism and lipid peroxidation
- Lipid metabolism and NAD(P)H
- Therapeutics targeting lipid metabolism and iron death
