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Advances in Molecular Research of Lipid Mediators
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Advances in Molecular Research of Lipid Mediators

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (20 October 2024) | Viewed by 4227

Special Issue Editors

Dr. Satoshi Ishii

E-Mail Website
Guest Editor
Department of Immunology, Akita University Graduate School of Medicine, Akita 010-8543, Japan
Interests: lysophosphatidic acid; LPA; G protein-coupled receptor; signal transduction; angiogenesis; lymphangiogenesis; mesenchymal stem cells; adipogenesis
Dr. Eric Camerer

E-Mail Website
Guest Editor
1. Paris Cardiovascular Research Center, Université Paris Cité, 75006 Paris, France
2. INSERM, 75015 Paris, France
Interests: sphingosine 1-phosphate; G protein-coupled receptors; signal transduction, vascular biology, vascular development; endothelial function; ischemic stroke; hemostasis

Special Issue Information

Dear Colleagues,

Lipids such as glycerolipids, sphingolipids and cholesterol are abundant intracellularly in biological membranes and fat droplets and extracellularly in lipoproteins. The production and degradation of these lipids are tightly regulated by many metabolic enzymes. Some lipid metabolic processes produce bioactive lipids (i.e., lipid mediators), which are responsible for various biological regulatory functions. Lipid mediators include arachidonic acid-derived molecules such as prostanoids and leukotrienes, as well as lysophospholipids such as lysophosphatidic acid (LPA) and sphingosine 1-phosphate (S1P). Platelet-activating factor (PAF), 2-arachidonoyl glycerol and fatty acids are also bioactive. Most of these lipid mediators bind to specific G protein-coupled receptors on the plasma membrane and mobilize second messengers within the cell to exert their effects. Others, such as cholesterol-derived steroid hormones, vitamin D and vitamin A, bind to nuclear receptors and regulate gene transcription. This Special Issue aims to update the current understandings about new roles of lipid mediators in health and diseases and to feature the latest progress in the molecular mechanisms of their functions. Studies on the metabolism of lipid mediators are also welcome. We invite you to contribute either in the form of original research articles or review articles.

Dr. Satoshi Ishii
Dr. Eric Camerer
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • prostaglandins
  • prostanoids
  • leukotrienes
  • phospholipids
  • lysophospholipids
  • endocannabinoids
  • fatty acids
  • steroids
  • GPCRs
  • signal transduction
  • nuclear receptors
  • metabolic enzymes

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Published Papers (3 papers)

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Research

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14 pages, 1673 KiB  
Article
Rising Lysophosphatidylcholine Levels Post-Hepatitis C Clearance
by Georg Peschel, Sabrina Krautbauer, Kilian Weigand, Jonathan Grimm, Marcus Höring, Gerhard Liebisch, Martina Müller and Christa Buechler
Int. J. Mol. Sci. 2024, 25(2), 1198; https://doi.org/10.3390/ijms25021198 - 18 Jan 2024
Cited by 1 | Viewed by 1246
Abstract
Hepatitis C virus (HCV) infection alters lysophosphatidylcholine (LPC) metabolism, enhancing viral infectivity and replication. Direct-acting antivirals (DAAs) effectively treat HCV and rapidly normalize serum cholesterol. In serum, LPC species are primarily albumin-bound but are also present in lipoprotein particles. This study aims to [...] Read more.
Hepatitis C virus (HCV) infection alters lysophosphatidylcholine (LPC) metabolism, enhancing viral infectivity and replication. Direct-acting antivirals (DAAs) effectively treat HCV and rapidly normalize serum cholesterol. In serum, LPC species are primarily albumin-bound but are also present in lipoprotein particles. This study aims to assess the impact of HCV eradication on serum LPC species levels in patients infected with HCV. Therefore, 12 different LPC species were measured by electrospray ionization tandem mass spectrometry (ESI-MS/MS) in the sera of 178 patients with chronic HCV infections at baseline, and in 176 of these patients after therapy with DAAs. All LPC species increased at 4 and 12 weeks post-initiation of DAA therapy. The serum profiles of the LPC species were similar before and after the viral cure. Patients with HCV and liver cirrhosis exhibited lower serum levels of all LPC species, except LPC 16:1, both before and after DAA treatment. Percentages of LPC 18:1 (relative to the total LPC level) were higher, and % LPC 22:5 and 22:6 were lower in cirrhotic compared to non-cirrhotic patients at baseline and at the end of therapy. LPC species levels inversely correlated with the model of end-stage liver disease score and directly with baseline and post-therapy albumin levels. Receiver operating characteristic curve analysis indicated an area under the curve of 0.773 and 0.720 for % LPC 18:1 (relative to total LPC levels) for classifying fibrosis at baseline and post-therapy, respectively. In summary, HCV elimination was found to increase all LPC species and elevated LPC 18:1 relative to total LPC levels may have pathological significance in HCV-related liver cirrhosis. Full article
(This article belongs to the Special Issue Advances in Molecular Research of Lipid Mediators)
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Review

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17 pages, 1252 KiB  
Review
Phospholipids, Sphingolipids, and Cholesterol-Derived Lipid Mediators and Their Role in Neurological Disorders
by Akhlaq A. Farooqui and Tahira Farooqui
Int. J. Mol. Sci. 2024, 25(19), 10672; https://doi.org/10.3390/ijms251910672 - 3 Oct 2024
Viewed by 890
Abstract
Neural membranes are composed of phospholipids, sphingolipids, cholesterol, and proteins. In response to cell stimulation or injury, the metabolism of lipids generates various lipid mediators, which perform many cellular functions. Thus, phospholipids release arachidonic acid or docosahexaenoic acid from the sn-2 position of [...] Read more.
Neural membranes are composed of phospholipids, sphingolipids, cholesterol, and proteins. In response to cell stimulation or injury, the metabolism of lipids generates various lipid mediators, which perform many cellular functions. Thus, phospholipids release arachidonic acid or docosahexaenoic acid from the sn-2 position of the glycerol moiety by the action of phospholipases A2. Arachidonic acid is a precursor for prostaglandins, leukotrienes, thromboxane, and lipoxins. Among these mediators, prostaglandins, leukotrienes, and thromboxane produce neuroinflammation. In contrast, lipoxins produce anti-inflammatory and pro-resolving effects. Prostaglandins, leukotrienes, and thromboxane are also involved in cell proliferation, differentiation, blood clotting, and blood vessel permeability. In contrast, DHA-derived lipid mediators are called specialized pro-resolving lipid metabolites (SPMs). They include resolvins, protectins, and maresins. These mediators regulate immune function by producing anti-inflammatory, pro-resolving, and cell protective effects. Sphingolipid-derived metabolites are ceramide, ceramide1-phosphate, sphingosine, and sphingosine 1 phosphate. They regulate many cellular processes, including enzyme activities, cell migration and adhesion, inflammation, and immunity. Cholesterol is metabolized into hydroxycholesterols and 7-ketocholesterol, which not only disrupts membrane fluidity, but also promotes inflammation, oxidative stress, and apoptosis. These processes lead to cellular damage. Full article
(This article belongs to the Special Issue Advances in Molecular Research of Lipid Mediators)
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12 pages, 1502 KiB  
Review
The Role of Phospholipid Alterations in Mitochondrial and Brain Dysfunction after Cardiac Arrest
by Rishabh C. Choudhary, Cyrus E. Kuschner, Jacob Kazmi, Liam Mcdevitt, Blanca B. Espin, Mohammed Essaihi, Mitsuaki Nishikimi, Lance B. Becker and Junhwan Kim
Int. J. Mol. Sci. 2024, 25(9), 4645; https://doi.org/10.3390/ijms25094645 - 24 Apr 2024
Cited by 1 | Viewed by 1521
Abstract
The human brain possesses three predominate phospholipids, phosphatidylcholine (PC), phosphatidylethanolamine (PE) and phosphatidylserine (PS), which account for approximately 35–40%, 35–40%, and 20% of the brain’s phospholipids, respectively. Mitochondrial membranes are relatively diverse, containing the aforementioned PC, PE, and PS, as well as phosphatidylinositol [...] Read more.
The human brain possesses three predominate phospholipids, phosphatidylcholine (PC), phosphatidylethanolamine (PE) and phosphatidylserine (PS), which account for approximately 35–40%, 35–40%, and 20% of the brain’s phospholipids, respectively. Mitochondrial membranes are relatively diverse, containing the aforementioned PC, PE, and PS, as well as phosphatidylinositol (PI) and phosphatidic acid (PA); however, cardiolipin (CL) and phosphatidylglycerol (PG) are exclusively present in mitochondrial membranes. These phospholipid interactions play an essential role in mitochondrial fusion and fission dynamics, leading to the maintenance of mitochondrial structural and signaling pathways. The essential nature of these phospholipids is demonstrated through the inability of mitochondria to tolerate alteration in these specific phospholipids, with changes leading to mitochondrial damage resulting in neural degeneration. This review will emphasize how the structure of phospholipids relates to their physiologic function, how their metabolism facilitates signaling, and the role of organ- and mitochondria-specific phospholipid compositions. Finally, we will discuss the effects of global ischemia and reperfusion on organ- and mitochondria-specific phospholipids alongside the novel therapeutics that may protect against injury. Full article
(This article belongs to the Special Issue Advances in Molecular Research of Lipid Mediators)
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