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The Role of Sphingolipids in Oxidative Stress
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The Role of Sphingolipids in Oxidative Stress

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

Deadline for manuscript submissions: closed (31 August 2021) | Viewed by 18074

Special Issue Editor

Dr. Norishi Ueda

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Guest Editor
Department of Pediatrics, Public Central Hospital of Matto Ishikawa, Ishikawa, Japan
Interests: apoptosis; Bcl-2 family proteins; cell death; cell signaling; ceramide; hepcidin; iron metabolism; mitochondria; oxidative stress; pediatric nephrology; reactive oxygen species; sphingolipids

Special Issue Information

Dear Colleagues,

Reactive oxygen species (ROS) derived from cellular oxidative metabolism are essential for normal cellular processes. However, excess production of ROS and/or reduced antioxidant defense system following diverse stimuli cause oxidative stress in various cells, tissues and organs. Sphingolipids, structural components of biological membranes, function as signaling molecules to regulate cellular function and cell fate in response to diverse stimuli including oxidative stress. Increasing evidence highlights a crosstalk between ROS-antioxidants and sphingolipid metabolism and signaling including the effect of ROS-antioxidants on a ceramide-sphingosine-1-phosphate rheostat which regulates mitochondrial function including Bcl-2 family proteins and downstream signaling pathways, leading to modulation of cellular function and cell fate in various types of oxidative stress-mediated disorders.
This Special Issue aims to provide new insights into the role of a crosstalk between ROS-antioxidants and sphingolipid metabolism and signaling as well as the molecular and cellular mechanisms used by sphingolipids in the regulation of physiological, pathophysiological and pathological processes during oxidative stress. Advances in the development of new drugs, therapeutic targets or strategies to modulate sphingolipid-regulating enzymes, receptors, mitochondrial function, sphingolipid-induced signaling pathways which contribute to the regulation of oxidative stress-mediated disorders are also welcome. We welcome your contribution in the form of original research articles, reviews or expert opinions on all aspects of the role of sphingolipids in the regulation of oxidative stress.

Dr. Norishi Ueda
Guest Editor

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

  • antioxidants
  • cell death (apoptosis, autophagy, necrosis)
  • Bcl-2 family proteins
  • cell proliferation/fibrosis/inflammation
  • ceramide
  • mitochondria
  • oxidative stress
  • reactive oxygen species
  • sphingolipid metabolism/signaling
  • sphingosine-1-phosphate

Published Papers (4 papers)

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Research

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18 pages, 2130 KiB  
Article
Novel Insight into the Serum Sphingolipid Fingerprint Characterizing Longevity
by Pietro Barbacini, Enrica Torretta, Beatrice Arosio, Evelyn Ferri, Daniele Capitanio, Manuela Moriggi and Cecilia Gelfi
Int. J. Mol. Sci. 2022, 23(5), 2428; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23052428 - 22 Feb 2022
Cited by 2 | Viewed by 1812
Abstract
Sphingolipids (SLs) are structural components of the lipid bilayer regulating cell functions. In biological fluids, their distribution is sex-specific and is at variance in aging and many disorders. The aim of this study is to identify SL species associated with the decelerated aging [...] Read more.
Sphingolipids (SLs) are structural components of the lipid bilayer regulating cell functions. In biological fluids, their distribution is sex-specific and is at variance in aging and many disorders. The aim of this study is to identify SL species associated with the decelerated aging of centenarians. SLs, extracted from serum of adults (Ad, 35–37 years old), aged (Ag, 75–77 years old) and centenarian (C, 105–107 years old) women were analyzed by LC-MS/MS in combination with mRNA levels in peripheral blood mononuclear cells (PBMCs) of SL biosynthetic enzymes. Results indicated in Ag and C vs. Ad a comparable ceramides (Cers) increase, whereas dihydroceramide (dhCer) decreased in C vs. Ad. Hexosylceramides (HexCer) species, specifically HexCer 16:0, 22:0 and 24:1 acyl chains, increased in C vs. Ag representing a specific trait of C. Sphingosine (Sph), dihydrosphingosine (dhSph), sphingosine-1-phosphate (S1P) and dihydrosphingosine-1-phosphate (dhS1P), increased both in Ag and C vs. Ad, with higher levels in Ag, indicating a SL fine-tuning associated with a reduced physiological decline in C. mRNA levels of enzymes involved in ceramide de novo biosynthesis increased in Ag whereas enzymes involved in sphingomyelin (SM) degradation increased in C. Collectively, results suggest that Ag produce Cers by de novo synthesis whereas C activate a protective mechanism degrading SMs to Cers converting it into glycosphingolipids. Full article
(This article belongs to the Special Issue The Role of Sphingolipids in Oxidative Stress)
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Review

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22 pages, 1059 KiB  
Review
Implications of Sphingolipid Metabolites in Kidney Diseases
by Shamroop kumar Mallela, Sandra Merscher and Alessia Fornoni
Int. J. Mol. Sci. 2022, 23(8), 4244; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23084244 - 11 Apr 2022
Cited by 14 | Viewed by 6220
Abstract
Sphingolipids, which act as a bioactive signaling molecules, are involved in several cellular processes such as cell survival, proliferation, migration and apoptosis. An imbalance in the levels of sphingolipids can be lethal to cells. Abnormalities in the levels of sphingolipids are associated with [...] Read more.
Sphingolipids, which act as a bioactive signaling molecules, are involved in several cellular processes such as cell survival, proliferation, migration and apoptosis. An imbalance in the levels of sphingolipids can be lethal to cells. Abnormalities in the levels of sphingolipids are associated with several human diseases including kidney diseases. Several studies demonstrate that sphingolipids play an important role in maintaining proper renal function. Sphingolipids can alter the glomerular filtration barrier by affecting the functioning of podocytes, which are key cellular components of the glomerular filtration barrier. This review summarizes the studies in our understanding of the regulation of sphingolipid signaling in kidney diseases, especially in glomerular and tubulointerstitial diseases, and the potential to target sphingolipid pathways in developing therapeutics for the treatment of renal diseases. Full article
(This article belongs to the Special Issue The Role of Sphingolipids in Oxidative Stress)
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45 pages, 3292 KiB  
Review
A Rheostat of Ceramide and Sphingosine-1-Phosphate as a Determinant of Oxidative Stress-Mediated Kidney Injury
by Norishi Ueda
Int. J. Mol. Sci. 2022, 23(7), 4010; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23074010 - 04 Apr 2022
Cited by 25 | Viewed by 4598
Abstract
Reactive oxygen species (ROS) modulate sphingolipid metabolism, including enzymes that generate ceramide and sphingosine-1-phosphate (S1P), and a ROS-antioxidant rheostat determines the metabolism of ceramide-S1P. ROS induce ceramide production by activating ceramide-producing enzymes, leading to apoptosis, while they inhibit S1P production, which promotes survival [...] Read more.
Reactive oxygen species (ROS) modulate sphingolipid metabolism, including enzymes that generate ceramide and sphingosine-1-phosphate (S1P), and a ROS-antioxidant rheostat determines the metabolism of ceramide-S1P. ROS induce ceramide production by activating ceramide-producing enzymes, leading to apoptosis, while they inhibit S1P production, which promotes survival by suppressing sphingosine kinases (SphKs). A ceramide-S1P rheostat regulates ROS-induced mitochondrial dysfunction, apoptotic/anti-apoptotic Bcl-2 family proteins and signaling pathways, leading to apoptosis, survival, cell proliferation, inflammation and fibrosis in the kidney. Ceramide inhibits the mitochondrial respiration chain and induces ceramide channel formation and the closure of voltage-dependent anion channels, leading to mitochondrial dysfunction, altered Bcl-2 family protein expression, ROS generation and disturbed calcium homeostasis. This activates ceramide-induced signaling pathways, leading to apoptosis. These events are mitigated by S1P/S1P receptors (S1PRs) that restore mitochondrial function and activate signaling pathways. SphK1 promotes survival and cell proliferation and inhibits inflammation, while SphK2 has the opposite effect. However, both SphK1 and SphK2 promote fibrosis. Thus, a ceramide-SphKs/S1P rheostat modulates oxidant-induced kidney injury by affecting mitochondrial function, ROS production, Bcl-2 family proteins, calcium homeostasis and their downstream signaling pathways. This review will summarize the current evidence for a role of interaction between ROS-antioxidants and ceramide-SphKs/S1P and of a ceramide-SphKs/S1P rheostat in the regulation of oxidative stress-mediated kidney diseases. Full article
(This article belongs to the Special Issue The Role of Sphingolipids in Oxidative Stress)
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23 pages, 3086 KiB  
Review
Macrophage Motility in Wound Healing Is Regulated by HIF-1α via S1P Signaling
by Islamy Rahma Hutami, Takashi Izawa, Tsendsuren Khurel-Ochir, Takuma Sakamaki, Akihiko Iwasa and Eiji Tanaka
Int. J. Mol. Sci. 2021, 22(16), 8992; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22168992 - 20 Aug 2021
Cited by 11 | Viewed by 4373
Abstract
Accumulating evidence indicates that the molecular pathways mediating wound healing induce cell migration and localization of cytokines to sites of injury. Macrophages are immune cells that sense and actively respond to disturbances in tissue homeostasis by initiating, and subsequently resolving, inflammation. Hypoxic conditions [...] Read more.
Accumulating evidence indicates that the molecular pathways mediating wound healing induce cell migration and localization of cytokines to sites of injury. Macrophages are immune cells that sense and actively respond to disturbances in tissue homeostasis by initiating, and subsequently resolving, inflammation. Hypoxic conditions generated at a wound site also strongly recruit macrophages and affect their function. Hypoxia inducible factor (HIF)-1α is a transcription factor that contributes to both glycolysis and the induction of inflammatory genes, while also being critical for macrophage activation. For the latter, HIF-1α regulates sphingosine 1-phosphate (S1P) to affect the migration, activation, differentiation, and polarization of macrophages. Recently, S1P and HIF-1α have received much attention, and various studies have been performed to investigate their roles in initiating and resolving inflammation via macrophages. It is hypothesized that the HIF-1α/S1P/S1P receptor axis is an important determinant of macrophage function under inflammatory conditions and during disease pathogenesis. Therefore, in this review, biological regulation of monocytes/macrophages in response to circulating HIF-1α is summarized, including signaling by S1P/S1P receptors, which have essential roles in wound healing. Full article
(This article belongs to the Special Issue The Role of Sphingolipids in Oxidative Stress)
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