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Although sphingolipids are ubiquitous components of cellular membranes, their abundance in cells is generally lower than glycerolipids or cholesterol, representing less than 20% of total lipid mass. Following their discovery in the brain—which contains the largest amounts of sphingolipids in the body—and first description in 1884 by J.L.W. Thudichum, sphingolipids have been overlooked for almost a century, perhaps due to their complexity and enigmatic nature. When sphingolipidoses were discovered, a series of inherited diseases caused by enzyme mutations involved in sphingolipid degradation returned to the limelight. The essential breakthrough came decades later, in the 1990s, with the discovery that sphingolipids were not just structural elements of cellular membranes but intra- and extracellular signaling molecules. It turned out that their lipid backbones, including ceramide and sphingosine-1-phosphate, had selective physiological functions. Thus, sphingolipids emerged as essential players in several pathologies including cancer, diabetes, neurodegenerative disorders, and autoimmune diseases. The present volume reflects upon the unexpectedly eclectic functions of sphingolipids in health, disease, and therapy. This fascinating lipid class will continue to be the subject of up-and-coming future discoveries, especially with regard to new therapeutic strategies.

S1P receptor --- inflammation --- S1P transporter --- spinster homolog 2 --- barrier dysfunction --- anxiety --- depression --- sphingolipids --- sphingomyelinase --- ceramidase --- Smpd1 --- acid sphingomyelinase --- forebrain --- depressive-like behavior --- anxiety-like behavior --- ceramide --- ceramides --- ceramidases --- neurodegenerative diseases --- infectious diseases --- sphingosine 1-phoshate --- sphingosine 1-phosphate receptor --- S1P1–5 --- sphingosine 1-phosphate metabolism --- sphingosine 1-phosphate antagonistst/inhibitors --- sphingosine 1-phosphate signaling --- stroke --- multiple sclerosis --- neurodegeneration --- fingolimod --- Sphingosine-1-phosphate --- obesity --- type 2 diabetes --- insulin resistance --- pancreatic β cell fate --- hypothalamus --- sphingosine-1-phosphate --- ischemia/reperfusion --- cardioprotection --- vasoconstriction --- coronary flow --- myocardial function --- myocardial infarct --- albumin --- type 1 diabetes --- beta-cells --- islets --- insulin --- cytokines --- S1P --- animal models --- cystic fibrosis --- autophagy --- myriocin --- Aspergillus fumigatus --- CLN3 disease --- Cln3Δex7/8 mice --- flupirtine --- allyl carbamate derivative --- apoptosis --- cancer --- gangliosides --- immunotherapy --- metastasis --- phenotype switching --- sphingosine 1-phosphate --- Sphingosine 1-phosphate (S1P) --- S1P-lyase (SGPL1) --- tau --- calcium --- histone acetylation --- hippocampus --- cortex --- astrocytes --- neurons --- sphingosine kinase --- G-protein-coupled receptors --- Gαq/11 --- n/a --- sphingosine kinase 1 --- SK1 --- microRNA --- transcription factor --- hypoxia --- long non-coding RNA --- S1P1-5

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Even though initially considered as a passive means for storing energy, lipids are now regarded as multifaceted molecules with crucial structural and functional activities. For instance, some of them play essential roles as key components of cell membranes whereas others act as signaling molecules in the regulation of cell homeostasis. In recent years, lipid research has attracted increasing interest because of the involvement of this class of compounds in human health. Indeed, a plethora of pathological conditions are characterized by alterations in lipid metabolism, such as cardiovascular diseases and brain disorders. This Special Issue is a collection of papers from different experts in lipid research, with the aim of providing new insights into the physiopathological involvement of lipids and their impact on human health. This collection also demonstrates the usefulness of interdisciplinary approaches in the development of novel methods to study and manipulate lipid metabolism, which may represent an attractive target for designing effective therapeutic strategies to counteract numerous pathologies.

Medicine --- neutral sphingomyelinase --- radiation --- sphingomyelin metabolism --- pathology --- cell signaling --- brain --- adipose tissue --- breast cancer --- epinephrine --- breast reconstruction --- epicardial fat thickness --- visceral fat thickness --- high-sensitivity c-reactive protein --- leptin --- gender --- female --- hippocampus --- frontal cortex --- adiponectin --- haptoglobin --- lipocalin --- BDNF --- synaptic proteins --- phosphatidylinositol 4,5-bisphosphate --- phospholipase C --- cholesterol --- high-cholesterol diet --- BET proteins --- cell proliferation --- epigenetics --- HMGCR --- JQ1 --- LDLr --- lipid metabolism --- SREBP --- TMEM97 --- atherosclerosis --- diabetes mellitus --- cardiovascular disease --- chronic inflammation --- hyperglycemia --- mutations --- lipid --- fatty acid --- glyceride --- steroid --- phospholipid --- oral drug absorption --- prodrug --- phospholipase A2 (PLA2) --- acid sphingomyelinase --- SOD --- liver --- eicosanoids --- ischemic stroke --- ischemia --- lipoproteins --- polyunsaturated fatty acids --- angiogenesis --- high-density lipoprotein --- endothelial cell --- metabolism --- metabolic reprogramming --- pulmonary fibrosis --- lipid mediators --- sphingolipids --- sphingosine-1-phosphate --- sphingosine kinase 1 --- prostaglandins --- lysophosphatidic acid --- autotaxin --- G-protein coupled receptors --- lysocardiolipin acyltransferase --- phospholipase D --- oxidized phospholipids --- DNA damage response --- double strand breaks --- ATM --- ionizing radiation --- metabolic stress --- oxidative stress --- p53 --- nuclear sphingolipids --- lipophagy --- lipolysis --- lipid droplets --- lipid storage diseases --- lipid metabolism diseases --- mTORC1 --- TFEB --- Cholesterol --- Fatty acids --- Lipid mediators --- Lipids --- Lipophagy --- Sphingolipids --- neutral sphingomyelinase --- radiation --- sphingomyelin metabolism --- pathology --- cell signaling --- brain --- adipose tissue --- breast cancer --- epinephrine --- breast reconstruction --- epicardial fat thickness --- visceral fat thickness --- high-sensitivity c-reactive protein --- leptin --- gender --- female --- hippocampus --- frontal cortex --- adiponectin --- haptoglobin --- lipocalin --- BDNF --- synaptic proteins --- phosphatidylinositol 4,5-bisphosphate --- phospholipase C --- cholesterol --- high-cholesterol diet --- BET proteins --- cell proliferation --- epigenetics --- HMGCR --- JQ1 --- LDLr --- lipid metabolism --- SREBP --- TMEM97 --- atherosclerosis --- diabetes mellitus --- cardiovascular disease --- chronic inflammation --- hyperglycemia --- mutations --- lipid --- fatty acid --- glyceride --- steroid --- phospholipid --- oral drug absorption --- prodrug --- phospholipase A2 (PLA2) --- acid sphingomyelinase --- SOD --- liver --- eicosanoids --- ischemic stroke --- ischemia --- lipoproteins --- polyunsaturated fatty acids --- angiogenesis --- high-density lipoprotein --- endothelial cell --- metabolism --- metabolic reprogramming --- pulmonary fibrosis --- lipid mediators --- sphingolipids --- sphingosine-1-phosphate --- sphingosine kinase 1 --- prostaglandins --- lysophosphatidic acid --- autotaxin --- G-protein coupled receptors --- lysocardiolipin acyltransferase --- phospholipase D --- oxidized phospholipids --- DNA damage response --- double strand breaks --- ATM --- ionizing radiation --- metabolic stress --- oxidative stress --- p53 --- nuclear sphingolipids --- lipophagy --- lipolysis --- lipid droplets --- lipid storage diseases --- lipid metabolism diseases --- mTORC1 --- TFEB --- Cholesterol --- Fatty acids --- Lipid mediators --- Lipids --- Lipophagy --- Sphingolipids