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Lipidology
Special Issues
Lipid Metabolism and Inflammation-Related Diseases
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Lipid Metabolism and Inflammation-Related Diseases

A special issue of Lipidology (ISSN 2813-7086).

Deadline for manuscript submissions: 31 March 2026 | Viewed by 1353

Special Issue Editors

Dr. Maria Pia Adorni

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Guest Editor
Department of Medicine and Surgery, University of Parma, Via Volturno 39/F, 43125 Parma, Italy
Interests: high-density lipoprotein (HDL) functions; cardiovascular pharmacology; atherosclerosis; inflammation; lipid metabolism; lipids in age-related diseases
Special Issues, Collections and Topics in MDPI journals
Dr. Bianca Papotti

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Guest Editor
Department of Food and Drug, University of Parma, Parco Area delle Scienze 27/A, 43124 Parma, Italy
Interests: high-density lipoprotein (HDL) functions; cardiovascular pharmacology; atherosclerosis; inflammation; lipid metabolism; lipids in neurodegenerative diseases

Special Issue Information

Dear Colleagues,

Over the past two decades, significant progress has been made in understanding the crosstalk between lipid metabolism and inflammatory responses, as well as their collective impact on chronic inflammatory diseases. Indeed, altered lipid metabolism is often associated with an abnormal immune response and, in turn, pro-inflammatory signalling can deeply affect lipid metabolism. In this context, targeting lipid metabolism has emerged as a promising therapeutic strategy to correct immune dysfunction in these conditions. However, translating these findings into clinical applications requires a deeper understanding of lipid metabolism across different immune cell subsets, as the regulatory mechanisms vary depending on cell type and disease context.

Based on this premise, this Special Issue provides researchers with an opportunity to publish both original research and review articles related to recent advances in understanding the role of lipids in immunometabolism, by investigating the mechanism by which lipids regulate immune cell function and, on the other hand, how inflammation impacts lipid metabolism in immune cells. Given their close relationship the high translational potential, we aim to particularly focus on the pharmacology of novel strategies with potential clinical use for preventing chronic inflammatory diseases, including metabolic diseases, autoimmune diseases, and cancer in the near future.

Dr. Maria Pia Adorni
Dr. Bianca Papotti
Guest Editors

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. Lipidology is an international peer-reviewed open access quarterly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1000 CHF (Swiss Francs). 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

  • inflammation
  • lipid metabolism
  • cholesterol
  • lipoproteins
  • immune cells
  • macrophage
  • inflammatory diseases

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Published Papers (2 papers)

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Research

14 pages, 268 KB  
Article
Human Monocyte-Derived Macrophages Acquire an Inflammatory Phenotype Relative to Risk Factors Typical of Atherogenic Dyslipidaemia
by Corinne D. Mack, Lily D. Quagliata, Rana Baraz, Sravanthi Naralashetty, Suat Dervish, Helen Williams, Stephen C. H. Li and Heather J. Medbury
Lipidology 2025, 2(4), 18; https://doi.org/10.3390/lipidology2040018 - 17 Oct 2025
Viewed by 155
Abstract
Background: Dyslipidaemia promotes atherosclerotic plaque formation. Plaques that are vulnerable to rupture have a higher proportion of inflammatory (M1:CD86) macrophages in their cap. Many plaque macrophages are derived from blood monocytes which have been exposed to elevated blood lipid levels. Here, we explored [...] Read more.
Background: Dyslipidaemia promotes atherosclerotic plaque formation. Plaques that are vulnerable to rupture have a higher proportion of inflammatory (M1:CD86) macrophages in their cap. Many plaque macrophages are derived from blood monocytes which have been exposed to elevated blood lipid levels. Here, we explored whether the inflammatory state of monocyte-derived macrophages is associated with blood lipid levels and assessed whether oxidised low-density lipoprotein (oxLDL) directly induces some of the observed changes. Method: Blood was collected from 20 individuals. Lipid profiles were measured, and monocytes differentiated into macrophages. Macrophage inflammatory state was assessed by flow cytometry for phenotypic markers (e.g., CD86 and CD163) and cytokine production: TNF, IL-1β, and IL-6. Furthermore, monocytes were isolated from 6 normo-lipidaemic individuals and cultured with oxLDL, followed by stimulation with LPS/IFNγ and assessment of the cytokine response. Results: The inflammatory phenotype acquired by macrophages (ex vivo) was related to levels of in vivo circulating lipids. Correlations for CD86/CD163 were found with CVD risk markers; most strongly with triglycerides (TG) and TG/HDL-C, but also with cholesterol/HDL-C and ApoB/ApoA1 and inversely with LDL particle size. Functionally, macrophage production of inflammatory cytokines (TNF and IL-1β) correlated with oxLDL levels and inversely with ApoA1. Macrophages differentiated from monocytes cultured with oxLDL produced significantly higher IL-1β but lower IL-10 (in response to LPS/IFNγ), compared to control cells. Conclusions: Monocyte-derived macrophages adopt an inflammatory phenotype relative to the levels of circulating lipid factors that are characteristic of atherogenic dyslipidaemia (such as high TG, TG/HDL-C and low LDL particle size), but not LDL-C. Full article
(This article belongs to the Special Issue Lipid Metabolism and Inflammation-Related Diseases)
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13 pages, 1842 KB  
Article
Pro-Inflammatory and Lipid Metabolism Dysregulating Effects of ANGPTL3 in THP-1 Macrophages
by Ilenia Milani, Ilaria Rossi, Giorgia Marodin, Maria Giovanna Lupo, Maria Pia Adorni, Francesca Zimetti and Nicola Ferri
Lipidology 2025, 2(3), 14; https://doi.org/10.3390/lipidology2030014 - 26 Jul 2025
Viewed by 694
Abstract
Background and aim: ANGPTL3 is a hepatokine acting as a negative regulator of lipoprotein lipase (LPL) through its N-terminal domain. Besides this activity, the C-terminal domain of ANGPTL3 interacts with integrin αVβ3. Since integrins are involved in inflammation and in the initiation of [...] Read more.
Background and aim: ANGPTL3 is a hepatokine acting as a negative regulator of lipoprotein lipase (LPL) through its N-terminal domain. Besides this activity, the C-terminal domain of ANGPTL3 interacts with integrin αVβ3. Since integrins are involved in inflammation and in the initiation of atherosclerotic plaque, the aim of our study was to evaluate the potential direct pro-inflammatory action of ANGPTL3 through the interaction of the fibrinogen-like domain and integrin αVβ3. Methods: We utilized cultured THP-1 human-derived macrophages and evaluated their pro-inflammatory phenotype in response to treatment with human recombinant ANGPTL3 (hANGPTL3). By Western blot, RT-qPCR, biochemical analysis, and ELISA assays, we determined the expression of genes and proteins involved in lipid metabolism and inflammatory response as well as intracellular cholesterol and triglyceride levels. In addition, we evaluated the effect of hANGPTL3 on the cellular cholesterol efflux process. Results: Incubation of THP-1-derived macrophages with 100 ng/mL of hANGPTL3 increased the mRNA expression of the pro-inflammatory cytokines IL-1β, IL-6, and TNFα (respectively, 1.87 ± 0.08-fold, 1.35 ± 0.11-fold, and 2.49 ± 0.43-fold vs. control). The secretion of TNFα, determined by an ELISA assay, was also induced by hANGPTL3 (1.98 ± 0.4-fold vs. control). The pro-inflammatory effect of hANGPTL3 was partially counteracted by co-treatment with the integrin αVβ3 inhibitor RGD peptide, reducing the mRNA levels of IL-1β (3.35 ± 0.35-fold vs. 2.54 ± 0.25-fold for hANGPTL3 vs. hANGPTL3 + RGD, respectively). Moreover, hANGPTL3 reduced cholesterol efflux to apoA-I, with a parallel increase in the intracellular triglyceride and cholesterol contents by 31.2 ± 2.8% and 20.0 ± 4.1%, respectively, compared to the control. Conclusions: ANGPTL3 is an important liver-derived regulator of plasma lipoprotein metabolism, and overall, our results add a new important pro-inflammatory activity of this circulating protein. This new function of ANGPTL3 could also be related to triglyceride and cholesterol accumulation into macrophages. Full article
(This article belongs to the Special Issue Lipid Metabolism and Inflammation-Related Diseases)
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