Submit to Lipidology Review for Lipidology Propose a Special Issue

Journal Menu

Journal Browser

► Journal Browser

Lipid Metabolism and Inflammation-Related Diseases

Special Issue Editors
Special Issue Information
Keywords
Benefits of Publishing in a Special Issue
Published Papers

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

Deadline for manuscript submissions: closed (31 May 2026) | Viewed by 7497

Share This Special Issue

Special Issue Editors

Dr. Maria Pia Adorni

E-Mail
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

E-Mail
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 250 words) can be sent to the Editorial Office for assessment.

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

Benefits of Publishing in a Special Issue

Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (7 papers)

Download All Papers

Order results

Result details

Show export options Show export options

Select all

Export citation of selected articles as:

Research

Jump to: Review

25 pages, 10710 KB

Open AccessArticle

PPARγ Deficiency in SZ95 Sebocytes Elicits Redox Stress and Impairs the Sequestosome/Autophagy-Mediated Clearance of Oxidized Lipids

by Alexandra Stiegler, Michaela Schirato, Ionela-Mariana Nagelreiter, Christina Bauer, Sarah Jelleschitz, Christopher Kremslehner, Christos C. Zouboulis, Dóra Kovács, Kinga Lénárt, Miriam Maiellaro, Emanuela Camera, Dániel Törőcsik and Florian Gruber

Lipidology 2026, 3(2), 18; https://doi.org/10.3390/lipidology3020018 - 20 May 2026

Viewed by 173

Abstract

Background/Objectives: Sebocytes, the primary cell type in sebaceous glands (SGs), produce a lipid mixture called sebum that is released onto the skin surface and is required for skin homeostasis. The lipid receptor Peroxisome Proliferator-Activated Receptor gamma (PPARγ) regulates sebocyte proliferation and lipid synthesis and is involved in acne development. As inhibition of PPARγ has been shown to reduce insulin-induced lipogenesis and Akt/mTOR signalling in SZ95 sebocytes, we here investigated the effects of PPARγ deletion on lipid homeostasis and autophagic stress responses and how the secretomes affect dermal fibroblasts. Methods: SZ95 sebocytes wildtype (WT) and PPARγ knockout (KO) were shifted to low serum and EGF-deficient conditions permissive for autophagy. Untargeted and targeted HPLC-MS/MS analyses were used to analyze native and oxidized lipids, respectively. Protein levels of LC3I/II and p62 were assessed using immunoblots and immunofluorescence microscopy to investigate the autophagic flux. Dermal fibroblasts were exposed to conditioned media. Results: In low serum culture media, KO SZ95 sebocytes displayed significantly altered levels of 23 lipid classes. We observed a significant increase in ether-linked fatty acids as components of complex lipids and detected elevated levels of phospholipid hydroperoxides and aldehydolipids in the KO sebocytes. KO SZ95 sebocytes failed to show the typical responses to lipoxidative stress, such as elevated p62 crosslinking or inclusion body formation, and had reduced LC3II/I ratios as compared to WT cells. PPARγ KO conditioned media promoted a trend towards an inflammatory fibroblast phenotype. Conclusions: These findings suggest that PPARγ in sebocytes may alter the lipidome, elevate redox stress, and affect the autophagic machinery, which could cause accumulation of oxidized lipids and other potentially harmful compounds in sebocytes. Full article

(This article belongs to the Special Issue Lipid Metabolism and Inflammation-Related Diseases)

► Show Figures

Figure 1

14 pages, 628 KB

Open AccessArticle

Evaluating the Effects of Full-Fat Yogurt Consumption on Circulating Inflammatory Biomarkers and Ex Vivo Peripheral Blood Mononuclear Cell Inflammatory Responses in a Randomized-Controlled Crossover Trial

by Victoria M. Taormina, Simonne Eisenhardt, Matthew P. Gilbert, C. Lawrence Kien, Matthew E. Poynter and Jana Kraft

Lipidology 2026, 3(1), 4; https://doi.org/10.3390/lipidology3010004 - 15 Jan 2026

Viewed by 1006

Abstract

Chronic, low-grade inflammation is a characteristic of metabolic diseases like type 2 diabetes. Despite recommendations to select low- or non-fat dairy foods over full-fat dairy foods for metabolic health, recent research suggests potential anti-inflammatory benefits of dairy fat consumption. We aimed to compare the systemic inflammatory tone (i.e., circulating inflammatory biomarker concentrations and ex vivo peripheral blood mononuclear cell inflammatory responses) of individuals with prediabetes after consuming diets with full-fat (3.25%) or non-fat yogurt. We hypothesized that short-term consumption of three daily full-fat yogurt servings beneficially affects inflammatory tone. Thirteen participants aged 45–75 years completed an eight-week randomized, double-masked, controlled crossover study. The two, three-week experimental diets comprised three daily servings of full-fat or non-fat yogurt and were each preceded by a one-week run-in diet. Following each diet, circulating inflammatory biomarkers and cytokine concentrations in the supernatants of peripheral blood mononuclear cells under control or lipopolysaccharide-stimulated conditions were measured. Compared with non-fat yogurt intake, circulating immature granulocyte concentrations were lower following full-fat yogurt intake, but there were no other differences in leukocyte concentrations. Circulating concentrations of cytokines or other inflammatory markers did not differ by diet. Cell supernatant interleukin-1β concentrations were lower following the full-fat yogurt diet under unstimulated conditions but were not different between diets under stimulated conditions. There were no differences by diet in supernatant concentrations of other cytokines under unstimulated or stimulated conditions. Together, minimal differences in inflammatory tone were observed following the short-term consumption of three daily servings of full-fat or non-fat yogurt in individuals with prediabetes. Full article

(This article belongs to the Special Issue Lipid Metabolism and Inflammation-Related Diseases)

► Show Figures

Graphical abstract

14 pages, 268 KB

Open AccessArticle

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 1453

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 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)

► Show Figures

Graphical abstract

13 pages, 1842 KB

Open AccessArticle

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 1771

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 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)

► Show Figures

Figure 1

Review

Jump to: Research

22 pages, 3271 KB

Open AccessReview

Lipidomics Approaches Reveal Tissue-Specific Lipidome Remodeling Induced by Micro- and Nanoplastic Exposure

by Priya Rathor, Ashutosh K. Tiwari, Damodara N. Kommi and Ratnasekhar CH

Lipidology 2026, 3(2), 16; https://doi.org/10.3390/lipidology3020016 - 7 May 2026

Viewed by 229

Abstract

Micro- and nanoplastics (MNPs) are increasingly recognized as frequent environmental pollutants with growing evidence of tissue-specific lipid disruption in exposed organisms. MNP exposure is unavoidable and has attracted global attention due to its potential public health and ecological security risks. Unlike earlier studies that emphasize oxidative stress and inflammation, recent findings show that lipids are among the earliest and most sensitive molecular targets of MNP exposure. Lipidomics investigations across animal models reveal consistent patterns of lipidome remodeling, including altered phospholipid composition, disrupted sphingolipid balance, increased neutral-lipid storage, and mitochondrial lipid damage in metabolically active tissues such as the liver, kidney, lung, adipose tissue, and brain. Mechanistically, MNPs perturb membrane bilayer organization, induce MUFA and PUFA peroxidation, and destabilize lysosomal and mitochondrial function. These alterations trigger cardiolipin oxidation, ceramide accumulation, lipid droplet biogenesis, and impaired lipophagy, which collectively promote metabolic stress, energy imbalance, and neurotoxic or hepatotoxic phenotypes. Despite the growing number of tissue-specific studies, a major gap remains in understanding systemic MNP toxicity. The present review uniquely emphasizes tissue-resolved lipidomic signatures to identify convergent pathways of lipid disruption and proposes a conceptual framework, the “Lipid–Stress Axis”, to explain how localized lipidome perturbations may propagate into broader physiological dysfunction. By integrating lipidomics with metabolomics, imaging, and systems-biology approaches, we highlight key lipid-based biomarkers, mechanistic insights, and research needs essential for improving risk assessment and developing mitigation strategies against MNP-induced lipid dysregulation. Full article

(This article belongs to the Special Issue Lipid Metabolism and Inflammation-Related Diseases)

► Show Figures

Figure 1

18 pages, 530 KB

Open AccessReview

Narrative Review of Human Adiposity: From Evolutionary Energy-Thriftiness and Ancestral Wellness to the Modern Inflammatory-Related Illness. The Role of Lifestyle Transition

by Roberto Carlos Burini

Lipidology 2026, 3(1), 11; https://doi.org/10.3390/lipidology3010011 - 18 Mar 2026

Viewed by 748

Abstract

Energy thriftiness and metabolic adaptations have had a crucial role in the emergence and spreading of the Homo lineage in the world. A higher-energy demand was required not only for the growing body mass, encephalization and human proliferation, but also for the survival adaptations to the environmental stresses. Because lean body mass lacks the energy-storage capacity required to supply the body’s demands, dedicated fat-storing cells originated. To feed such fat stores, the hominid evolution developed “meat-adaptive” genes to detect, digest and metabolize higher fat diets, and body-fat stores can be affected by lifestyle through hormonal-controlled daily energy balance. In energy surplus conditions, hypertrophy and hyperplasia of adipocytes can occur, with hypertrophic adipocyte signaling both a neo-adipocyte differentiation (leading to hyperplasia) and a local macrophage density (resident + infiltrated macrophages) for fat surplus scavenging. Adiposity-induced inflammation is caused by fat-overstored (hypertrophied) adipocytes that may operate as an overactive endocrine organ secreting an array of pro-inflammatory adipokines that, in combination with resident-macrophage activity and infiltrated blood-recruited, monocyte-derived macrophages, amplify the inflammatory process by spurting pro-inflammatory cytokines into the bloodstream. From an evolutionary perspective, obese humans represent a natural selection overexpressing the “thrifty” genes evolved for efficient food collection and fat deposition intended to help in survival in prolonged periods of famine. However, genetically speaking, obesity is a polygenic multifactorial disorder. Considering the rapidity of obesity-epidemic growth worldwide, epigenetic sets forth the key assumption of the mismatch between our human genome molded over thousands of generations, coping with the unprecedented dietary and physical conditions. Consequently, obesity would be due to our evolutionary-adapted polygenic-charge expressed by a deteriorated lifestyle characterized by high energy-dense food intake coupled with a reduction in caloric expenditure stemming from new mobility-reducing technologies. As a model of lifestyle change (LiSM), our 28-year on-going longitudinal study (“Moving for Health”) has shown effectiveness in the reduction not only of obesity but especially of its comorbidities, in a (10 week to 3 year) length-dependent LiSM. However, a disappointing progressive decrease in compliance with the study has been observed and attributed to the resistance of people to change their actual “obesogenic” lifestyle, basically represented by the individuals’ demand for labor-saving technologies and convenient, affordable, palatable foods. Full article

(This article belongs to the Special Issue Lipid Metabolism and Inflammation-Related Diseases)

► Show Figures

Figure 1

26 pages, 795 KB

Open AccessReview

Dysregulated Skeletal Muscle Lipid Handling Drives Myocardial Mitochondrial Dysfunction Through ASK-1 and PPARγ Signaling

by Preyangsee Dutta and Dwaipayan Saha

Lipidology 2026, 3(1), 5; https://doi.org/10.3390/lipidology3010005 - 31 Jan 2026

Viewed by 1008

Abstract

Cardiovascular disease is the leading cause of mortality in insulin-resistant individuals, with metabolic cardiomyopathy preceding overt heart failure in a substantial proportion of patients with diabetes. Skeletal muscle accounts for approximately 40% of body mass and nearly 80% of insulin-stimulated glucose disposal, positioning it as a major determinant of systemic lipid flux. Dysregulation of lipid droplet dynamics, lipolysis, and fatty acid trafficking in skeletal muscle alters circulating lipid availability and promotes ectopic lipid deposition and mitochondrial stress in the myocardium. Intramyocellular lipid handling is governed by coordinated actions of lipid droplets, perilipin proteins (PLIN2 and PLIN3), adipose triglyceride lipase (ATGL), and diacylglycerol acyltransferases (DGAT1/2), which together regulate the rate and composition of fatty acid release into the circulation. Impaired coupling between intramyocellular lipid droplet turnover and mitochondrial oxidation in insulin-resistant muscle increases circulating free fatty acids, reducing cardiac oxidative capacity. In response, the myocardium undergoes mitochondrial lipid remodeling, including alterations in cardiolipin composition that impair cristae structure and electron transport chain efficiency. Excess lipid exposure activates apoptosis signal-regulating kinase-1 (ASK-1), promoting cardiomyocyte apoptosis and inflammatory signaling, while peroxisome proliferator-activated receptor gamma (PPARγ) modulates lipid uptake, storage, and mitochondrial oxidation in a context-dependent manner. This review integrates skeletal muscle–cardiac lipid crosstalk with ASK-1 and PPARγ signaling to define mechanisms linking peripheral insulin resistance to early myocardial dysfunction and to identify targets for intervention before irreversible cardiac remodeling develops. Full article

(This article belongs to the Special Issue Lipid Metabolism and Inflammation-Related Diseases)

► Show Figures

Journal Menu

Journal Browser

Lipid Metabolism and Inflammation-Related Diseases

Share This Special Issue

Special Issue Editors

Special Issue Information

Keywords

Benefits of Publishing in a Special Issue

Published Papers (7 papers)

Research

Review

Further Information

Guidelines

MDPI Initiatives

Follow MDPI