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Lipid Molecules in Inflammation and Chronic Diseases
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Lipid Molecules in Inflammation and Chronic Diseases

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

Deadline for manuscript submissions: closed (31 January 2022) | Viewed by 28498

Special Issue Editor

Prof. Dr. Yong-Moon Lee

E-Mail Website
Guest Editor
College of Pharmacy, Chungbuk National University, Cheongju, Chungbuk 28644, Korea
Interests: sphingolipid metabolites; inflammation; chronic diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Endogenous lipid molecules in the wide range of biological processes are involved in the lipid class of prostaglandins, leukotrienes, sphingolipids, steroids, phospholipids and acylglycerol derivatives.  Such diverse lipids regulate inflammatory responses positively or negatively. The inflammatory signaling reversely regulates lipid metabolism and thus alter lipids composition in targeted organs such as liver, adipose tissue, skeletal muscle and macrophage. 

Therefore, this special section is focused on the interconnected networks from lipid signaling, inflammatory signaling and the etiology related to lifestyle-related diseases, cancer, diabetes, obesity and atherosclerosis etc. Particularly, the research on the signaling pathways that connect inflammation to lipid metabolism will be welcomed.

Prof. Dr. Yong-Moon Lee
Guest Editor

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Published Papers (6 papers)

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Research

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20 pages, 3034 KiB  
Article
Methylxanthines Induce a Change in the AD/Neurodegeneration-Linked Lipid Profile in Neuroblastoma Cells
by Daniel Janitschke, Anna Andrea Lauer, Cornel Manuel Bachmann, Jakob Winkler, Lea Victoria Griebsch, Sabrina Melanie Pilz, Elena Leoni Theiss, Heike Sabine Grimm, Tobias Hartmann and Marcus Otto Walter Grimm
Int. J. Mol. Sci. 2022, 23(4), 2295; https://doi.org/10.3390/ijms23042295 - 18 Feb 2022
Cited by 6 | Viewed by 4334
Abstract
Alzheimer’s disease (AD) is characterized by an increased plaque burden and tangle accumulation in the brain accompanied by extensive lipid alterations. Methylxanthines (MTXs) are alkaloids frequently consumed by dietary intake known to interfere with the molecular mechanisms leading to AD. Besides the fact [...] Read more.
Alzheimer’s disease (AD) is characterized by an increased plaque burden and tangle accumulation in the brain accompanied by extensive lipid alterations. Methylxanthines (MTXs) are alkaloids frequently consumed by dietary intake known to interfere with the molecular mechanisms leading to AD. Besides the fact that MTX consumption is associated with changes in triglycerides and cholesterol in serum and liver, little is known about the effect of MTXs on other lipid classes, which raises the question of whether MTX can alter lipids in a way that may be relevant in AD. Here we have analyzed naturally occurring MTXs caffeine, theobromine, theophylline, and the synthetic MTXs pentoxifylline and propentofylline also used as drugs in different neuroblastoma cell lines. Our results show that lipid alterations are not limited to triglycerides and cholesterol in the liver and serum, but also include changes in sphingomyelins, ceramides, phosphatidylcholine, and plasmalogens in neuroblastoma cells. These changes comprise alterations known to be beneficial, but also adverse effects regarding AD were observed. Our results give an additional perspective of the complex link between MTX and AD, and suggest combining MTX with a lipid-altering diet compensating the adverse effects of MTX rather than using MTX alone to prevent or treat AD. Full article
(This article belongs to the Special Issue Lipid Molecules in Inflammation and Chronic Diseases)
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18 pages, 4945 KiB  
Article
A Dansyl-Modified Sphingosine Kinase Inhibitor DPF-543 Enhanced De Novo Ceramide Generation
by Maftuna Shamshiddinova, Shokhid Gulyamov, Hee-Jung Kim, Seo-Hyeon Jung, Dong-Jae Baek and Yong-Moon Lee
Int. J. Mol. Sci. 2021, 22(17), 9190; https://doi.org/10.3390/ijms22179190 - 25 Aug 2021
Cited by 4 | Viewed by 2669
Abstract
Sphingosine-1-phosphate (S1P) synthesized by sphingosine kinase (SPHK) is a signaling molecule, involved in cell proliferation, growth, differentiation, and survival. Indeed, a sharp increase of S1P is linked to a pathological outcome with inflammation, cancer metastasis, or angiogenesis, etc. In this regard, SPHK/S1P axis [...] Read more.
Sphingosine-1-phosphate (S1P) synthesized by sphingosine kinase (SPHK) is a signaling molecule, involved in cell proliferation, growth, differentiation, and survival. Indeed, a sharp increase of S1P is linked to a pathological outcome with inflammation, cancer metastasis, or angiogenesis, etc. In this regard, SPHK/S1P axis regulation has been a specific issue in the anticancer strategy to turn accumulated sphingosine (SPN) into cytotoxic ceramides (Cers). For these purposes, there have been numerous chemicals synthesized for SPHK inhibition. In this study, we investigated the comparative efficiency of dansylated PF-543 (DPF-543) on the Cers synthesis along with PF-543. DPF-543 deserved attention in strong cytotoxicity, due to the cytotoxic Cers accumulation by ceramide synthase (CerSs). DPF-543 exhibited dual actions on Cers synthesis by enhancing serine palmitoyltransferase (SPT) activity, and by inhibiting SPHKs, which eventually induced an unusual environment with a high amount of 3-ketosphinganine and sphinganine (SPA). SPA in turn was consumed to synthesize Cers via de novo pathway. Interestingly, PF-543 increased only the SPN level, but not for SPA. In addition, DPF-543 mildly activates acid sphingomyelinase (aSMase), which contributes a partial increase in Cers. Collectively, a dansyl-modified DPF-543 relatively enhanced Cers accumulation via de novo pathway which was not observed in PF-543. Our results demonstrated that the structural modification on SPHK inhibitors is still an attractive anticancer strategy by regulating sphingolipid metabolism. Full article
(This article belongs to the Special Issue Lipid Molecules in Inflammation and Chronic Diseases)
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17 pages, 11637 KiB  
Article
Anti-Inflammatory Effect of Auranofin on Palmitic Acid and LPS-Induced Inflammatory Response by Modulating TLR4 and NOX4-Mediated NF-κB Signaling Pathway in RAW264.7 Macrophages
by Hyun Hwangbo, Seon Yeong Ji, Min Yeong Kim, So Young Kim, Hyesook Lee, Gi-Young Kim, Suhkmann Kim, JaeHun Cheong and Yung Hyun Choi
Int. J. Mol. Sci. 2021, 22(11), 5920; https://doi.org/10.3390/ijms22115920 - 31 May 2021
Cited by 35 | Viewed by 5083
Abstract
Chronic inflammation, which is promoted by the production and secretion of inflammatory mediators and cytokines in activated macrophages, is responsible for the development of many diseases. Auranofin is a Food and Drug Administration-approved gold-based compound for the treatment of rheumatoid arthritis, and evidence [...] Read more.
Chronic inflammation, which is promoted by the production and secretion of inflammatory mediators and cytokines in activated macrophages, is responsible for the development of many diseases. Auranofin is a Food and Drug Administration-approved gold-based compound for the treatment of rheumatoid arthritis, and evidence suggests that auranofin could be a potential therapeutic agent for inflammation. In this study, to demonstrate the inhibitory effect of auranofin on chronic inflammation, a saturated fatty acid, palmitic acid (PA), and a low concentration of lipopolysaccharide (LPS) were used to activate RAW264.7 macrophages. The results show that PA amplified LPS signals to produce nitric oxide (NO) and various cytokines. However, auranofin significantly inhibited the levels of NO, monocyte chemoattractant protein-1, and pro-inflammatory cytokines, such as interleukin (IL)-1β, tumor necrosis factor-α, and IL-6, which had been increased by co-treatment with PA and LPS. Moreover, the expression of inducible NO synthase, IL-1β, and IL-6 mRNA and protein levels increased by PA and LPS were reduced by auranofin. In particular, the upregulation of NADPH oxidase (NOX) 4 and the translocation of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) induced by PA and LPS were suppressed by auranofin. The binding between the toll-like receptor (TLR) 4 and auranofin was also predicted, and the release of NO and cytokines was reduced more by simultaneous treatment with auranofin and TLR4 inhibitor than by auranofin alone. In conclusion, all these findings suggested that auranofin had anti-inflammatory effects in PA and LPS-induced macrophages by interacting with TLR4 and downregulating the NOX4-mediated NF-κB signaling pathway. Full article
(This article belongs to the Special Issue Lipid Molecules in Inflammation and Chronic Diseases)
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Review

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11 pages, 263 KiB  
Review
Cholesterol Transport Dysfunction and Its Involvement in Atherogenesis
by Anastasia V. Poznyak, Dmitry A. Kashirskikh, Vasily N. Sukhorukov, Vladislav Kalmykov, Andrey V. Omelchenko and Alexander N. Orekhov
Int. J. Mol. Sci. 2022, 23(3), 1332; https://doi.org/10.3390/ijms23031332 - 25 Jan 2022
Cited by 25 | Viewed by 4405
Abstract
Atherosclerosis is the cause of the development of serious cardiovascular disorders, leading to disability and death. Numerous processes are involved in the pathogenesis of atherosclerosis, including inflammation, endothelial dysfunction, oxidative stress, and lipid metabolism disorders. Reverse transport of cholesterol is a mechanism presumably [...] Read more.
Atherosclerosis is the cause of the development of serious cardiovascular disorders, leading to disability and death. Numerous processes are involved in the pathogenesis of atherosclerosis, including inflammation, endothelial dysfunction, oxidative stress, and lipid metabolism disorders. Reverse transport of cholesterol is a mechanism presumably underlying the atheroprotective effect of high-density lipoprotein. In this review, we examined disorders of cholesterol metabolism and their possible effect on atherogenesis. We paid special attention to the reverse transport of cholesterol. Transformed cholesterol metabolism results in dyslipidemia and early atherosclerosis. Reverse cholesterol transport is an endogenous mechanism by which cells export cholesterol and maintain homeostasis. It is known that one of the main factors leading to the formation of atherosclerotic plaques on the walls of blood vessels are multiple modifications of low-density lipoprotein, and the formation of foam cells following them. Full article
(This article belongs to the Special Issue Lipid Molecules in Inflammation and Chronic Diseases)
14 pages, 4437 KiB  
Review
Bile Acid Signaling in Inflammatory Bowel Disease
by Mariusz A. Bromke and Małgorzata Krzystek-Korpacka
Int. J. Mol. Sci. 2021, 22(16), 9096; https://doi.org/10.3390/ijms22169096 - 23 Aug 2021
Cited by 36 | Viewed by 5926
Abstract
Inflammatory bowel disease is a chronic, idiopathic and complex condition, which most often manifests itself in the form of ulcerative colitis or Crohn’s disease. Both forms are associated with dysregulation of the mucosal immune system, compromised intestinal epithelial barrier, and dysbiosis of the [...] Read more.
Inflammatory bowel disease is a chronic, idiopathic and complex condition, which most often manifests itself in the form of ulcerative colitis or Crohn’s disease. Both forms are associated with dysregulation of the mucosal immune system, compromised intestinal epithelial barrier, and dysbiosis of the gut microbiome. It has been observed for a long time that bile acids are involved in inflammatory disorders, and recent studies show their significant physiological role, reaching far beyond being emulsifiers helping in digestion of lipids. Bile acids are also signaling molecules, which act, among other things, on lipid metabolism and immune responses, through several nuclear and membrane receptors in hepatocytes, enterocytes and cells of the immune system. Gut microbiota homeostasis also seems to be affected, directly and indirectly, by bile acid metabolism and signaling. This review summarizes recent advances in the field of bile acid signaling, studies of inflamed gut microbiome, and the therapeutic potential of bile acids in the context of inflammatory bowel disease. Full article
(This article belongs to the Special Issue Lipid Molecules in Inflammation and Chronic Diseases)
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32 pages, 983 KiB  
Review
Mitochondrial Lipid Homeostasis at the Crossroads of Liver and Heart Diseases
by Siarhei A. Dabravolski, Evgeny E. Bezsonov, Mirza S. Baig, Tatyana V. Popkova and Alexander N. Orekhov
Int. J. Mol. Sci. 2021, 22(13), 6949; https://doi.org/10.3390/ijms22136949 - 28 Jun 2021
Cited by 22 | Viewed by 5089
Abstract
The prevalence of NAFLD (non-alcoholic fatty liver disease) is a rapidly increasing problem, affecting a huge population around the globe. However, CVDs (cardiovascular diseases) are the most common cause of mortality in NAFLD patients. Atherogenic dyslipidemia, characterized by plasma hypertriglyceridemia, increased small dense [...] Read more.
The prevalence of NAFLD (non-alcoholic fatty liver disease) is a rapidly increasing problem, affecting a huge population around the globe. However, CVDs (cardiovascular diseases) are the most common cause of mortality in NAFLD patients. Atherogenic dyslipidemia, characterized by plasma hypertriglyceridemia, increased small dense LDL (low-density lipoprotein) particles, and decreased HDL-C (high-density lipoprotein cholesterol) levels, is often observed in NAFLD patients. In this review, we summarize recent genetic evidence, proving the diverse nature of metabolic pathways involved in NAFLD pathogenesis. Analysis of available genetic data suggests that the altered operation of fatty-acid β-oxidation in liver mitochondria is the key process, connecting NAFLD-mediated dyslipidemia and elevated CVD risk. In addition, we discuss several NAFLD-associated genes with documented anti-atherosclerotic or cardioprotective effects, and current pharmaceutical strategies focused on both NAFLD treatment and reduction of CVD risk. Full article
(This article belongs to the Special Issue Lipid Molecules in Inflammation and Chronic Diseases)
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