Lipid Signaling in Human Disease

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Lipids".

Deadline for manuscript submissions: 10 December 2025 | Viewed by 728

Special Issue Editors


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Guest Editor
Department of Biology, Norwegian University of Science and Technology, Trondheim, Norway
Interests: lipid signaling; inflammatory mechanisms; phospholipase A2 (PLA2); fibrotic disease

E-Mail Website
Guest Editor
Department of Biology, Norwegian University of Science and Technology, Trondheim, Norway
Interests: inflammation regulator; lipid signaling mediators; cytosolic phospholipase A2α (cPLA2α); psoriasis; macrophage

Special Issue Information

Dear Colleagues,

Lipids are fundamental components of cellular membranes, essential energy stores, and critical participants in cell signaling and gene regulatory mechanisms. They are essential contributors to the delicate balance between physiology and pathology in living systems that are often overlooked in protein-centric biological research. Phospholipids, broadly classified as glycerophospholipids and sphingolipids, are the major constituents of cell membranes. They can be cleaved by phospholipases to produce potent lipid signaling molecules that regulate innate and adaptive immune responses, as well as cell fate decisions. Consequently, dysregulated lipid signaling contributes to the pathogenesis of a range of illnesses, including chronic inflammatory and fibrotic conditions, cardiovascular disease, neurodegenerative disorders, and cancer. The successful therapeutic targeting of lipid signaling pathways could therefore have a large societal impact.

The focus of this Special Issue is on the contribution of lipid signaling to the pathogenesis of human disease, particularly non-communicable illnesses, and we invite both review articles and original research articles relevant to this topic. We particularly encourage the submission of basic research that advances knowledge of the contribution of membrane-derived lipid signaling molecules to cellular disease mechanisms, as well as pharmacological, translational, and clinical research articles.

Prof. Dr. Berit Johansen
Dr. Felicity Ashcroft
Guest Editors

Manuscript Submission Information

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Keywords

  • lipid signaling pathways
  • membrane-derived lipid signaling molecules
  • inflammation mechanisms
  • cellular disease mechanisms
  • phospholipids
  • phospholipases
  • glycerophospholipids
  • sphingolipids

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Published Papers (1 paper)

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Research

19 pages, 7031 KB  
Article
Integrated Multi-Omics Investigation of Gypenosides’ Mechanisms in Lowering Hepatic Cholesterol
by Qin Jiang, Tao Yang, Hao Yang, Yi Chen, Yuan Xiong, Lin Qin, Qianru Zhang, Daopeng Tan, Xingdong Wu, Yongxia Zhao, Jian Xie and Yuqi He
Biomolecules 2025, 15(8), 1205; https://doi.org/10.3390/biom15081205 - 21 Aug 2025
Viewed by 546
Abstract
(1) Objective: This study aimed to systematically elucidate the molecular mechanisms by which gypenosides (GP), a major active component of Gynostemma pentaphyllum, ameliorate hypercholesterolemia by modulating the hepatic steroidogenesis pathway, and to identify key therapeutic targets. (2) Methods: We established a high-fat [...] Read more.
(1) Objective: This study aimed to systematically elucidate the molecular mechanisms by which gypenosides (GP), a major active component of Gynostemma pentaphyllum, ameliorate hypercholesterolemia by modulating the hepatic steroidogenesis pathway, and to identify key therapeutic targets. (2) Methods: We established a high-fat diet (HFD)-induced hypercholesterolemia (HC) mouse model and performed GP intervention. An integrated multi-omics approach, combining transcriptomics and proteomics, was utilized to comprehensively analyze GP’s effects on the expression of genes and proteins associated with hepatic cholesterol synthesis, transport, and steroid hormone metabolism. (3) Results: HFD induced significant dysregulation, with 48 steroidogenesis pathway-related genes and 35 corresponding proteins exhibiting altered expression in HC mouse livers. GP treatment remarkably reversed these HFD-induced abnormalities, significantly restoring the expression levels of 42 genes and 14 proteins. Multi-omics integration identified seven critical genes/proteins—Cyp3a25, Fdft1, Tm7sf2, Hmgcs1, Fdps, Mvd, and Pmvk—that were consistently and significantly regulated by GP at both transcriptional and translational levels. Furthermore, correlation analyses demonstrated that Cyp3a25 was significantly negatively correlated with serum total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C), whereas Fdft1, Tm7sf2, Hmgcs1, Fdps, Mvd, and Pmvk showed significant positive correlations. (4) Conclusions: GP effectively ameliorates cholesterol dyshomeostasis through a multi-targeted mechanism in the liver. It inhibits endogenous cholesterol synthesis by downregulating key enzymes (Hmgcs1, Fdft1, Pmvk, Mvd, Fdps, Tm7sf2), promotes cholesterol efflux and transport (upregulating Abca1, ApoB), and accelerates steroid hormone metabolism (upregulating Cyp3a11, Cyp3a25). These findings provide robust scientific evidence for the development of GP as a safe and effective novel therapeutic agent for hypercholesterolemia. Full article
(This article belongs to the Special Issue Lipid Signaling in Human Disease)
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