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The Twist and Turn of Lipids in Human Diseases 2.0
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The Twist and Turn of Lipids in Human Diseases 2.0

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 March 2025) | Viewed by 6979

Special Issue Editor

Dr. Manoj Kumar Pandey

E-Mail Website
Guest Editor
Department of Pediatrics, University of Cincinnati, Cincinnati, OH, USA
Interests: genetic and neurodegenerative diseases; complement; cytokines; innate and adaptive immunity
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is a continuation of our previous Special Issues "The Twist and Turn of Lipids in Human Diseases" (https://www.mdpi.com/journal/ijms/special_issues/lipids_hum_dis).

Lipids are vital for running several cellular and metabolic functions. However, excess tissue accumulation and/or reaction to immune and neurological cells trigger visceral and brain-immune inflammation. This leads to tissue damage and organ failure in many inflammatory conditions, including atherosclerosis, diabetes, fatty liver, allergy, asthma, autoimmune, neurodegenerative, and lysosomal storage sicknesses, e.g., Gaucher, Fabry, Tay-Sachs, Sandhoff, Niemann-Pick, Farbar, Krabbe, Metachromatic Leukodystrophy, and the Women, disorders. An adequate understanding of the battle between lipids and the immune system, which processes the tissue inflammation in indicated disorders, still eludes the medical community. Hence, the current research topics will seek to better understand the lipid-mediated biological processes that drive tissue damage and organ failure in human diseases. The outcome of these studies may also open new avenues for disease interventions.

Dr. Manoj Kumar Pandey
Guest Editor

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Related Special Issue

Published Papers (5 papers)

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Research

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17 pages, 4608 KiB  
Article
Proteomics Profiling Reveals Pharmaceutical Excipient PEG400 Induces Nuclear-Receptor-Activation-Affected Lipid Metabolism and Metabolic Enzyme Expression
by Mei Zhao, Siyuan Cao, Dan Yang, Leyuan Shang, Ye Hang, Pengjiao Wang, Shuo Zhang, Chaoji Li, Min Zhang and Xiuli Gao
Int. J. Mol. Sci. 2025, 26(4), 1732; https://doi.org/10.3390/ijms26041732 - 18 Feb 2025
Viewed by 721
Abstract
PEG400 is widely used as a pharmaceutical excipient in the biomedical field. Increasing evidence suggests that PEG400 is not an inert drug carrier; it can influence the activity of various drug-metabolizing enzymes and transporters, thereby affecting the in vivo process of drugs. It [...] Read more.
PEG400 is widely used as a pharmaceutical excipient in the biomedical field. Increasing evidence suggests that PEG400 is not an inert drug carrier; it can influence the activity of various drug-metabolizing enzymes and transporters, thereby affecting the in vivo process of drugs. It can also alleviate obesity and adipose tissue inflammation induced by a high-fat diet. In this study, we employed proteomics to investigate the impact of PEG400 on hepatic protein expression in rats. We found that over 40 metabolic enzymes were altered, with UDP-glucuronosyltransferase 1a9 (Ugt1a9) showing the most significant upregulation. This observation is consistent with our previous findings. KEGG pathway enrichment analysis revealed that PEG400 influences retinol metabolism, steroid hormone biosynthesis, drug metabolism, bile secretion, fatty acid degradation, peroxisome proliferator-activated receptor (PPAR) signaling pathway, and pentose and glucuronate interconversions. Western blot and molecular docking were used to quantitatively analyze related proteins. The results demonstrated that PEG400 promotes the metabolism of retinol to produce retinoic acid; enhances bile secretion by upregulating bile acid synthesis and transporter proteins; and activates the PPARα signaling pathway to regulate the expression of fat metabolism-related proteins, thereby reducing lipid accumulation. Furthermore, as natural ligands for nuclear receptors, retinoic acid and bile acids may activate nuclear receptors and initiate the regulation of target gene expression. We found upregulation of the nuclear receptors PPARα, retinoid X receptor alpha (RXRα), and pregnane X receptor (PXR). RXRα can form a dimer with PPARα or PXR to regulate the expression of target genes, which may explain the changes in the expression of numerous metabolic enzymes. This study provides a comprehensive understanding of the effects of PEG400 on liver metabolism in rats, reveals its potential biological functions, and offers new insights into the application and development of PEG400. Full article
(This article belongs to the Special Issue The Twist and Turn of Lipids in Human Diseases 2.0)
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17 pages, 4156 KiB  
Article
Effect of METTL3 Gene on Lipopolysaccharide Induced Damage to Primary Small Intestinal Epithelial Cells in Sheep
by Yanjun Duan, Xiaoyang Lv, Xiukai Cao and Wei Sun
Int. J. Mol. Sci. 2024, 25(17), 9316; https://doi.org/10.3390/ijms25179316 - 28 Aug 2024
Viewed by 1292
Abstract
Newborn lambs are susceptible to pathogenic bacterial infections leading to enteritis, which affects their growth and development and causes losses in sheep production. It has been reported that N6-methyladenosine (m6A) is closely related to innate immunity, but the effect of m6A on sheep [...] Read more.
Newborn lambs are susceptible to pathogenic bacterial infections leading to enteritis, which affects their growth and development and causes losses in sheep production. It has been reported that N6-methyladenosine (m6A) is closely related to innate immunity, but the effect of m6A on sheep small intestinal epithelial cells (IECs) and the mechanism involved have not been elucidated. Here, we investigated the effects of m6A on lipopolysaccharide (LPS)-induced inflammatory responses, apoptosis and oxidative stress in primary sheep IECs. First, the extracted IECs were identified by immunofluorescence using the epithelial cell signature protein cytokeratin 18 (CK18), and the cellular activity of IECs induced by different concentrations of LPS was determined by the CCK8 assay. Meanwhile, LPS could induce the upregulation of mRNA and protein levels of IECs cytokines IL1β, IL6 and TNFα and the apoptosis marker genes caspase-3, caspase-9, Bax, and apoptosis rate, reactive oxygen species (ROS) levels and mRNA levels of CAT, Mn-SOD and CuZn-SOD, and METTL3 were found to be upregulated during induction. It was hypothesized that METTL3 may have a potential effect on the induction of IECs by LPS. Overexpression and knockdown of METTL3 in IECs revealed that a low-level expression of METTL3 could reduce the inflammatory response, apoptosis and ROS levels in LPS-induced IECs to some extent. The results suggest that METTL3 may be a genetic marker for potential resistance to cellular damage. Full article
(This article belongs to the Special Issue The Twist and Turn of Lipids in Human Diseases 2.0)
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Review

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16 pages, 4356 KiB  
Review
5-Methylcytosine Methylation-Linked Hippo Pathway Molecular Interactions Regulate Lipid Metabolism
by Lichen Du, Rui Gao and Zhi Chen
Int. J. Mol. Sci. 2025, 26(6), 2560; https://doi.org/10.3390/ijms26062560 - 12 Mar 2025
Viewed by 543
Abstract
5-methylcytosine (5mC) is a common form of DNA methylation, essentially acting as an epigenetic modification that regulates gene expression by affecting the binding of transcription factors to DNA or by recruiting proteins that make it difficult to recognize and transcribe genes. 5mC methylation [...] Read more.
5-methylcytosine (5mC) is a common form of DNA methylation, essentially acting as an epigenetic modification that regulates gene expression by affecting the binding of transcription factors to DNA or by recruiting proteins that make it difficult to recognize and transcribe genes. 5mC methylation is present in eukaryotes in a variety of places, such as in CpG islands, within gene bodies, and in regions of repetitive sequences, whereas in prokaryotic organisms, it is mainly present in genomic DNA. The Hippo pathway is a highly conserved signal transduction pathway, which is extremely important in cell proliferation and death, controlling the size of tissues and organs and regulating cell differentiation, in addition to its important regulatory roles in lipid synthesis, transport, and catabolism. Lipid metabolism is an important part of various metabolic pathways in the human body, and problems in lipid metabolism are related to abnormalities in key enzymes, related proteins, epigenetic inheritance, and certain specific amino acids, which are the key factors affecting its proper regulation. In this article, we will introduce the molecular mechanisms of 5mC methylation and the Hippo signaling pathway, and the possibility of their co-regulation of lipid metabolism, with the aim of providing new ideas for further research and novel therapeutic modalities for lipid metabolism and a reference for the development and exploration of related research. Full article
(This article belongs to the Special Issue The Twist and Turn of Lipids in Human Diseases 2.0)
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39 pages, 2047 KiB  
Review
Complement System and Adhesion Molecule Skirmishes in Fabry Disease: Insights into Pathogenesis and Disease Mechanisms
by Albert Frank Magnusen and Manoj Kumar Pandey
Int. J. Mol. Sci. 2024, 25(22), 12252; https://doi.org/10.3390/ijms252212252 - 14 Nov 2024
Cited by 1 | Viewed by 1664
Abstract
Fabry disease is a rare X-linked lysosomal storage disorder caused by mutations in the galactosidase alpha (GLA) gene, resulting in the accumulation of globotriaosylceramide (Gb3) and its deacetylated form, globotriaosylsphingosine (Lyso-Gb3) in various tissues and fluids throughout the body. This pathological [...] Read more.
Fabry disease is a rare X-linked lysosomal storage disorder caused by mutations in the galactosidase alpha (GLA) gene, resulting in the accumulation of globotriaosylceramide (Gb3) and its deacetylated form, globotriaosylsphingosine (Lyso-Gb3) in various tissues and fluids throughout the body. This pathological accumulation triggers a cascade of processes involving immune dysregulation and complement system activation. Elevated levels of complement 3a (C3a), C5a, and their precursor C3 are observed in the plasma, serum, and tissues of patients with Fabry disease, correlating with significant endothelial cell abnormalities and vascular dysfunction. This review elucidates how the complement system, particularly through the activation of C3a and C5a, exacerbates disease pathology. The activation of these pathways leads to the upregulation of adhesion molecules, including vascular cell adhesion molecule 1 (VCAM1), intercellular adhesion molecule 1 (ICAM1), platelet and endothelial cell adhesion molecule 1 (PECAM1), and complement receptor 3 (CR3) on leukocytes and endothelial cells. This upregulation promotes the excessive recruitment of leukocytes, which in turn exacerbates disease pathology. Targeting complement components C3a, C5a, or their respective receptors, C3aR (C3a receptor) and C5aR1 (C5a receptor 1), could potentially reduce inflammation, mitigate tissue damage, and improve clinical outcomes for individuals with Fabry disease. Full article
(This article belongs to the Special Issue The Twist and Turn of Lipids in Human Diseases 2.0)
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29 pages, 2887 KiB  
Review
Targeting Lipid Metabolism in Cancer Stem Cells for Anticancer Treatment
by Manish Kumar Singh, Sunhee Han, Sungsoo Kim and Insug Kang
Int. J. Mol. Sci. 2024, 25(20), 11185; https://doi.org/10.3390/ijms252011185 - 17 Oct 2024
Cited by 4 | Viewed by 2165
Abstract
Cancer stem cells (CSCs), or tumor-initiating cells (TICs), are small subpopulations (0.0001–0.1%) of cancer cells that are crucial for cancer relapse and therapy resistance. The elimination of each CSC is essential for achieving long-term remission. Metabolic reprogramming, particularly lipids, has a significant impact [...] Read more.
Cancer stem cells (CSCs), or tumor-initiating cells (TICs), are small subpopulations (0.0001–0.1%) of cancer cells that are crucial for cancer relapse and therapy resistance. The elimination of each CSC is essential for achieving long-term remission. Metabolic reprogramming, particularly lipids, has a significant impact on drug efficacy by influencing drug diffusion, altering membrane permeability, modifying mitochondrial function, and adjusting the lipid composition within CSCs. These changes contribute to the development of chemoresistance in various cancers. The intricate relationship between lipid metabolism and drug resistance in CSCs is an emerging area of research, as different lipid species play essential roles in multiple stages of autophagy. However, the link between autophagy and lipid metabolism in the context of CSC regulation remains unclear. Understanding the interplay between autophagy and lipid reprogramming in CSCs could lead to the development of new approaches for enhancing therapies and reducing tumorigenicity in these cells. In this review, we explore the latest findings on lipid metabolism in CSCs, including the role of key regulatory enzymes, inhibitors, and the contribution of autophagy in maintaining lipid homeostasis. These recent findings may provide critical insights for identifying novel pharmacological targets for effective anticancer treatment. Full article
(This article belongs to the Special Issue The Twist and Turn of Lipids in Human Diseases 2.0)
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