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The Role of Lipids in Human Health

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

Deadline for manuscript submissions: 20 September 2025 | Viewed by 738

Special Issue Editors


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Guest Editor
Department of Pharmacological and Biomedical Sciences “Rodolfo Paoletti”, University of Milan, Via D. Trentacoste 2, 20134 Milan, Italy
Interests: lipid biochemistry; lipidomics; omega-3 fatty acids; sphingolipid metabolism; cancer biology; applied nutrition; space life sciences
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E-Mail Website
Guest Editor
Department of Pharmacological and Biomedical Sciences “Rodolfo Paoletti”, University of Milan, Via D. Trentacoste 2, 20134 Milan, Italy
Interests: lipid biochemistry; lipidomics; omega-3 fatty acids; sphingolipid metabolism; cancer biology; applied nutrition; space life sciences

Special Issue Information

Dear Colleagues,

Lipids are a heterogeneous class of biomolecules whose altered metabolism is one of the key features for human health and diseases. Lipids are essential for energy storage, membrane structure, and synthesis of bioactive molecules. Through membrane dynamics, lipid-protein and lipid-lipid interactions, lipids and their metabolites modulate cell signaling, proliferation and differentiation, inflammatory and degenerative processes, and immune response.

Lipids are an essential component for the homeostatic function in human health. Every organ and tissue in the body depends on lipids for some of its most essential functions, and dysregulation in their metabolism and profile might be correlated with several human diseases.

As a result, this Special Issue will discuss new developments in our knowledge of how lipids and their metabolites affect human health and pathological states. In addition, this Special Issue represents an opportunity to present new molecular and/or cellular mechanisms and propose new targets to ameliorate human health and counteract diseases.

Dr. Angela Maria Rizzo
Dr. Irma Colombo
Guest Editors

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Keywords

  • lipids
  • lipidomics
  • fatty acids
  • sphingolipids
  • steroids
  • metabolism

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Published Papers (1 paper)

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Research

12 pages, 2921 KiB  
Article
Fenofibrate Treatment Inhibits Very-Low-Density Lipoprotein Transport Vesicle Formation by Reducing Sar1b Protein Expression
by Kayli Winterfeldt, Fahim Rejanur Tasin, Vandana Sekhar and Shadab A. Siddiqi
Int. J. Mol. Sci. 2025, 26(10), 4720; https://doi.org/10.3390/ijms26104720 - 15 May 2025
Viewed by 440
Abstract
Dyslipidemia is a well-known risk factor in the development and progression of atherosclerosis. VLDL plays a crucial role in maintaining lipid homeostasis; however, even minor fluctuations in its production, intracellular trafficking, and secretion can contribute to the progression of atherosclerosis. Fenofibrate is an [...] Read more.
Dyslipidemia is a well-known risk factor in the development and progression of atherosclerosis. VLDL plays a crucial role in maintaining lipid homeostasis; however, even minor fluctuations in its production, intracellular trafficking, and secretion can contribute to the progression of atherosclerosis. Fenofibrate is an FDA-approved drug that effectively lowers plasma triglycerides and VLDL-associated cholesterol while simultaneously increasing HDL levels. Although fenofibrate is a known PPARα agonist with several proposed mechanisms for its lipid-altering effects, its impact on the intracellular trafficking of VLDL has not yet been investigated. We observed that treatment of HepG2 cells with 50 µM of fenofibrate resulted in a significant reduction in VLDL secretion, as evidenced by a significant decrease in the secretion of 3H-labeled TAG, fluorescent TAG, and ApoB100 protein into the media. Using confocal microscopy to monitor VLDL intracellular trafficking, we observed a distinct change in VLDL triglyceride localization, suggesting delayed transport through the endoplasmic reticulum and Golgi. An immunoblot analysis revealed a decrease in Sar1B protein expression, a key regulator of COPII protein recruitment, which is essential for VTV formation and intracellular VLDL trafficking, the rate-limiting step in VLDL secretion. Our data reveal a novel mechanism by which fenofibrate alters the lipid profile by interfering with intracellular VLDL trafficking in hepatocytes. Full article
(This article belongs to the Special Issue The Role of Lipids in Human Health)
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