Reprint
Sphingolipids
From Pathology to Therapeutic Perspectives - A Themed Honorary Issue to Prof. Lina Obeid
Edited by
July 2021
292 pages
- ISBN978-3-03943-957-7 (Hardback)
- ISBN978-3-03943-958-4 (PDF)
This book is a reprint of the Special Issue Sphingolipids: From Pathology to Therapeutic Perspectives - A Themed Honorary Issue to Prof. Lina Obeid that was published in
Biology & Life Sciences
Medicine & Pharmacology
Summary
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.
Format
- Hardback
License
© 2022 by the authors; CC BY-NC-ND license
Keywords
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; inflammation; 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; sphingolipids; S1P; animal models; cystic fibrosis; sphingolipids; autophagy; myriocin; Aspergillus fumigatus; sphingolipids; neurodegeneration; ceramide; CLN3 disease; Cln3Δex7/8 mice; flupirtine; allyl carbamate derivative; apoptosis; cancer; ceramide; 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; sphingosine-1-phosphate; G-protein-coupled receptors; Gαq/11; n/a; sphingosine kinase 1; SK1; microRNA; transcription factor; hypoxia; long non-coding RNA