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Biomedicines
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Lipid and Lipoprotein Metabolism in Human Health and Diseases—the 2nd...
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Lipid and Lipoprotein Metabolism in Human Health and Diseases—the 2nd Edition

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 15 April 2025 | Viewed by 3311

Special Issue Editor

Dr. Ilenia Calcaterra

E-Mail Website
Guest Editor
Dipartimento di Medicina Clinica e Chirurgia, Università degli Studi di Napoli Federico II, 80131 Naples, Italy
Interests: familial hypercholesterolemia; cardiovascular disease lipoprotein; lipidomic
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Collegues,

Lipids are essential components of cellular membranes and lipoproteins. Lipids play many essential roles in cellular functions, including cellular barriers, membrane matrices, signaling pathways and energy storage.

Lipid and lipoprotein metabolism represent a complex set of chemical reactions involving liver, bowel, and endothelial compartments. Specific proteins and enzymes are involved in this process and, when deficient, they cause human diseases (e.g., familial hypercholesterolemia (FH) or familial chylomicronemia syndrome (FCS)).

Since the 1950s, lipids have been extracted from cells or tissues and total lipid extracts have been analyzed by chromatography and mass spectrometry. Over the years, the detailed study of lipid and lipoprotein metabolism has led to greater knowledge of the pathophysiological mechanisms of dyslipidemias. Furthermore, the identification of new therapeutic targets has allowed for the treatment of pathologies that had been ignored until a few years ago (e.g., PCSK9, ANGPTL-3, ApoCIII and MTP inhibition).

New perspectives are emerging from novel laboratory approaches, in particular omics studies. The results of these studies are promising in identifying novel biomarkers that will help in the diagnosis, prognosis and treatment of human diseases (e.g., cancer and atherosclerotic vascular diseases). Moreover, a promising application is the characterization of endpoints in clinical trials, which remains a major issue in drug development.

The aim of the Special Issue is to give an update on new evidence in studies on lipid metabolism and multi-omics evaluations and to clarify the molecular features of human disease, particularly in hereditary lipid disorders. The present Special Issue is addressed towards basic and clinical research.  Reviews and original research articles are welcome. The topics included in the Special Issue are the following:

  • The role of lipids in various physiological processes and pathophysiological mechanisms of human disease;
  • The evaluation of lipidome modifications following pharmacological intervention;
  • Novel laboratory approaches (multi-omics) to human disease, in particular lipid disorders and atherosclerosis.

Dr. Ilenia Calcaterra
Guest Editor

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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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

  • lipoprotein
  • lipid metabolism
  • lipidome
  • lipidomics
  • mass spectrometry
  • hereditary lipid disorders
  • familial hypercholesterolemia
  • omic
  • metabolomic
  • genomic

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Related Special Issue

Published Papers (3 papers)

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Research

12 pages, 2277 KiB  
Article
Lymph Node Adiposity and Metabolic Dysfunction-Associated Steatotic Liver Disease
by Jessica M. Rubino, Natalie Yanzi Ring, Krishna Patel, Xiaoqing Xia, Todd A. MacKenzie and Roberta M. diFlorio-Alexander
Biomedicines 2025, 13(1), 80; https://doi.org/10.3390/biomedicines13010080 - 1 Jan 2025
Viewed by 799
Abstract
Objective: Metabolic dysfunction-associated steatotic liver disease (MASLD), previously known as the most common chronic liver disease, is soon to be the leading indication for liver transplantation; however, the diagnosis may remain occult for decades. There is a need for biomarkers that identify [...] Read more.
Objective: Metabolic dysfunction-associated steatotic liver disease (MASLD), previously known as the most common chronic liver disease, is soon to be the leading indication for liver transplantation; however, the diagnosis may remain occult for decades. There is a need for biomarkers that identify patients at risk for MASLD and patients at risk for disease progression to optimize patient management and outcomes. Lymph node adiposity (LNA) is a novel marker of adiposity identified within axillary lymph nodes on screening mammography. Recent studies have demonstrated a correlation between LNA and cardiometabolic disease and cardiovascular disease risk. This study aimed to investigate the association between MASLD and LNA to evaluate the potential of mammographic LNA to serve as an imaging biomarker of MASLD. Methods: We identified women with pathology-proven MASLD who had a liver biopsy and a screening mammogram within 12 months of the liver biopsy. This resulted in a sample size of 161 women for final analysis that met the inclusion criteria. We evaluated lymph node adiposity through multiple measurements of the largest axillary lymph node visualized on mammography and correlated LNA with MASLD histology. Statistical analysis using univariable and multivariable logistic regression and odds ratios was performed using R version 4.1.0 (2021), the R Foundation for Statistical Computing Platform. Results: We found a significant association between MASLD and mammographic LNA, defined as lymph node (LN) length > 16 mm (p = 0.0004) that remained significant after adjusting for clinical factors, including body mass index (BMI). We additionally found a significant association between LNA and metabolic dysfunction-associated steatohepatitis (MASH), identified via liver biopsy (p = 0.0048). Conclusions: Mammographic lymph node adiposity may serve as a helpful imaging biomarker of MASLD in women who have an elevated risk for the development of MASH. Full article
(This article belongs to the Special Issue Lipid and Lipoprotein Metabolism in Human Health and Diseases—the 2nd Edition)
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Figure 1

Figure 1
<p>Variable lymph node size and morphology on mammographic medio-lateral oblique (MLO) views of the axilla. (<b>A</b>) Normal axillary lymph nodes measuring 8–11 mm (dotted line) with small physiologic “fatty notch” of lucent hilar fat (circle). (<b>B</b>) Fat-enlarged axillary lymph nodes measuring 25–29 mm (dotted line) due to increased lucent hilar fat (circle).</p> Full article ">Figure 2
<p>Data collection.</p> Full article ">Figure 3
<p>Lymph node (LN) measurements obtained: a—LN length, b—Hilar length, c—LN width, d—hilar width.</p> Full article ">Figure 4
<p>Performance of lymph node adiposity for predicting steatosis. (<b>A</b>) LN measurements alone yielded AUC of 61.9% to 68.7%. (<b>B</b>) LN measurements combined with clinical variables yielded AUC of 80.4% to 83.5%.</p> Full article ">
14 pages, 1799 KiB  
Article
The Potential Causal Association of Apolipoprotein A and B and Age-Related Macular Degeneration: A Mendelian Randomisation Study
by Young Lee and Je Hyun Seo
Biomedicines 2024, 12(12), 2828; https://doi.org/10.3390/biomedicines12122828 - 12 Dec 2024
Viewed by 912
Abstract
Background/Objectives: Research has suggested a potential relationship between apolipoproteins A (ApoA) and B (ApoB) and age-related macular degeneration (AMD). This study explored the potential causal relationship between ApoA/ApoB levels and AMD/AMD subtypes using two-sample Mendelian randomisation (MR). Methods: We selected 308 single nucleotide [...] Read more.
Background/Objectives: Research has suggested a potential relationship between apolipoproteins A (ApoA) and B (ApoB) and age-related macular degeneration (AMD). This study explored the potential causal relationship between ApoA/ApoB levels and AMD/AMD subtypes using two-sample Mendelian randomisation (MR). Methods: We selected 308 single nucleotide polymorphisms (SNPs) for ApoA and 198 SNPs for ApoB from the UK Biobank data. Summary statistics for AMD were collected from the genome-wide association study of the FinnGen project. We performed two-sample MR to assess the causal effects of ApoA/ApoB on AMD and its subtypes. Potential confounders, including body mass index, C-reactive protein level, and smoking status, were assessed using a multivariable MR analysis. Results: ApoA showed a significant causal association with AMD (odds ratio [OR] = 1.14, 95% confidence interval [CI] = 1.05–1.25, p = 0.003) and was linked to both dry (p = 0.004) and wet (p = 0.025) AMD. ApoB showed a decreasing trend in dry AMD risk (p = 0.074), though not significant, and was not associated with overall or wet AMD. The multivariable MR analysis showed no significant association of ApoA with any AMD subtype (p > 0.05). ApoB decreased dry AMD risk (OR = 0.89, 95% CI = 0.80–0.99, p = 0.039), with trends for overall and wet AMD that were not significant (p = 0.070 and p = 0.091, respectively). Conclusions: These findings suggest that ApoB is associated with lower AMD risk, particularly for dry AMD. Further research is needed to clarify lipid biomarker’s role as AMD risk factors. Full article
(This article belongs to the Special Issue Lipid and Lipoprotein Metabolism in Human Health and Diseases—the 2nd Edition)
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Figure 1

Figure 1
<p>A schematic diagram of the Mendelian randomisation study design. BMI, body mass index; CRP, C-reactive protein; SNP, single-nucleotide polymorphism; ApoA, apolipoprotein A; ApoB, apolipoprotein B; and AMD, age-related macular degeneration. Solid lines represent the presence of an association, while dashed lines indicate the absence of an association.</p> Full article ">Figure 2
<p>Forest plots of the causal associations of apolipoprotein A with AMD and AMD subtypes. AMD, age-related macular degeneration; SNP, single-nucleotide polymorphism; OR, odds ratio; CI, confidence interval; IVW, inverse-variance weighted; MR, Mendelian randomisation; SIMEX, simulation extrapolation; PRESSO, pleiotropy residual sum and outlier.</p> Full article ">Figure 3
<p>Forest plots of the causal associations of apolipoprotein B with AMD and AMD subtypes. AMD, age-related macular degeneration; SNP, single-nucleotide polymorphism; OR, odds ratio; CI, confidence interval; IVW, inverse-variance weighted; MR, Mendelian randomisation; SIMEX, simulation extrapolation; PRESSO, pleiotropy residual sum and outlier.</p> Full article ">Figure 4
<p>Scatter plots of MR tests assessing the effects of apolipoproteins A and B on AMD and AMD subtypes. Scatter plot indicating the effects of apolipoproteins A on AMD (<b>A</b>), dry AMD (<b>B</b>), and wet AMD (<b>C</b>) as well as those of apolipoproteins B on AMD (<b>D</b>), dry AMD (<b>E</b>), and wet AMD (<b>F</b>). Light blue, dark blue, light green, and dark green regression lines represent the IVW, MR-Egger, MR-Egger (SIMEX), and weighted median estimates, respectively. The slope of each line reflects the causal effect estimated by the corresponding method. Each dot corresponds to a SNP, with the x-axis representing the association between the SNP and the exposure, and the y-axis representing the association between the SNP and the outcome. Red dots indicate outliers identified by the MR-pleiotropy residual sum and outlier analysis. AMD, age-related macular degeneration; IVW, inverse-variance weighted; MR, Mendelian randomisation; SIMEX, simulation extrapolation; SNP, single-nucleotide polymorphism.</p> Full article ">
9 pages, 806 KiB  
Article
Assessment of Platelet Aggregation and Thrombin Generation in Patients with Familial Chylomicronemia Syndrome Treated with Volanesorsen: A Cross-Sectional Study
by Ilenia Lorenza Calcaterra, Renata Santoro, Nicoletta Vitelli, Ferdinando Cirillo, Guido D’Errico, Cornelia Guerrino, Giovanna Cardiero, Maria Donata Di Taranto, Giuliana Fortunato, Gabriella Iannuzzo and Matteo Nicola Dario Di Minno
Biomedicines 2024, 12(9), 2017; https://doi.org/10.3390/biomedicines12092017 - 4 Sep 2024
Cited by 2 | Viewed by 938
Abstract
Background: The antisense oligonucleotide against APOC3 mRNA volanesorsen was recently introduced to treat Familial Chylomicronemia Syndrome (FCS). Cases of decreased platelet count are reported among patients treated with volanesorsen. The aim of the study was to evaluate platelet function and thrombin generation (TG) [...] Read more.
Background: The antisense oligonucleotide against APOC3 mRNA volanesorsen was recently introduced to treat Familial Chylomicronemia Syndrome (FCS). Cases of decreased platelet count are reported among patients treated with volanesorsen. The aim of the study was to evaluate platelet function and thrombin generation (TG) assessment in FCS patients receiving volanesorsen. We performed a cross-sectional study on FCS patients treated with volanesorsen. Methods: Changes in platelet count PLC were assessed from baseline to Tw12 and Tw36. To assess TG, samples were processed by CAT (with PPP-reagent LOW). The results were expressed by the thrombogram graphic (thrombin variation over time); LagTime; endogenous thrombin potential (ETP); peak; time to reach peak (ttpeak), StartTail and Velocity Index. Platelet aggregation was assessed by testing different agonists using the turbidimetry method. Results: Four FCS patients and four matched healthy controls were included in the present study. Changes in PLC were 30% at Tw12 and 34% at Tw36. Thrombin generation results showed values in the normal range (for patients and controls, respectively, LagTime:10.42 ± 4.40 and 9.25 ± 0.99; ttPeak:14.33 ± 4.01 and 13.10 ± 0.67; StartTail: 32.13 ± 3.54 and 29.46 ± 1.69; Velocity Index: 20.21 ± 3.63 and 33.05 ± 13.21; ETP: 599.80 ± 73.47 and 900.2 ± 210.99; peak value: 76.84 ± 1.07 and 123.30 ± 39.45) and no significant difference between cases and controls. Platelet aggregation test showed values in range, with no significant difference compared to healthy controls. Conclusions: Our study showed for the first time that no significant changes in general hemostasis assessed by TG and in platelet function were observed in FCS patients receiving volanesorsen. Full article
(This article belongs to the Special Issue Lipid and Lipoprotein Metabolism in Human Health and Diseases—the 2nd Edition)
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Figure 1

Figure 1
<p>Individual percent changes in PLC from baseline to T12w and T36w (<b>a</b>). Cumulative percent changes in PLC from baseline to T12w and T36w (<b>b</b>).</p> Full article ">Figure 2
<p>Outcome of thrombin generation (CAT) shown for each patient.</p> Full article ">
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