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Apolipoproteins and Lipoproteins in Health and Disease, 3rd Edition
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Apolipoproteins and Lipoproteins in Health and Disease, 3rd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 August 2025 | Viewed by 6023

Special Issue Editor

Dr. Joan Carles Escolà-Gil

E-Mail Website
Guest Editor
Institut d’Investigacions Biomèdiques (IIB) Sant Pau, CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Barcelona, Spain
Interests: atherosclerosis; cholesterol; genetically-modified mice; HDL; lipoproteins
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleague,

We are pleased to support and edit a new Special Issue for the International Journal of Molecular Sciences, entitled “Apolipoproteins and Lipoproteins in Health and Disease 3.0”, which is a continuation of our previous "Apolipoproteins in Health and Disease" and "Apolipoproteins and Lipoproteins in Health and Disease 2.0" Special Issues.

Although apolipoproteins were originally recognized as major determinants in lipoprotein metabolism and cardiovascular disease, the multiple apolipoprotein and lipoprotein classes and subclasses have emerged as relevant participants in multiple biological processes and pathophysiological pathways involved in diabetes, cancer, obesity, neurodegenerative disorders, and inflammatory as well as infectious diseases.

Led by Dr. Joan Carles Escolà-Gil and Dr. Noemí Rotllan, and assisted by our Topical Advisory Panel Member Dr. Marina Canyelles, this Special Issue aims to publish timely and informative findings on the molecular aspects of apolipoproteins (including isoforms and post-translational modifications) in addition to their influence on health and disease risk. Manuscripts of original research and reviews will be welcome.

Dr. Joan Carles Escolà-Gil
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • apolipoproteins
  • Alzheimer's disease
  • atherosclerosis
  • cancer
  • cholesterol
  • diabetes
  • inflammation
  • obesity
  • lipid metabolism
  • lipoproteins

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Related Special Issues

Published Papers (5 papers)

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Editorial

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5 pages, 450 KiB  
Editorial
Challenges and Future Directions in Lipoprotein Measurement for Atherosclerosis Prevention and Treatment
by Tomokazu Konishi
Int. J. Mol. Sci. 2024, 25(24), 13247; https://doi.org/10.3390/ijms252413247 - 10 Dec 2024
Viewed by 705
Abstract
Atherosclerosis can cause severe damage to the heart, brain, and other vital organs [...] Full article
(This article belongs to the Special Issue Apolipoproteins and Lipoproteins in Health and Disease, 3rd Edition)
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Research

Jump to: Editorial

12 pages, 4157 KiB  
Article
Overexpression of Apolipoprotein A-I Alleviates Insulin Resistance in MASLD Mice Through the PPARα Pathway
by Yifan Wang, Yudian Zhang and Yutong Wang
Int. J. Mol. Sci. 2025, 26(3), 1051; https://doi.org/10.3390/ijms26031051 - 26 Jan 2025
Viewed by 686
Abstract
Insulin resistance (IR) is one of the important causes of metabolic dysfunction-associated steatotic liver disease (MASLD). Apolipoprotein A-I (apoA-I) is secreted primarily by hepatocytes and plays an essential role in reverse cholesterol transport. Our previous studies revealed that apoA-I can mitigate the progression [...] Read more.
Insulin resistance (IR) is one of the important causes of metabolic dysfunction-associated steatotic liver disease (MASLD). Apolipoprotein A-I (apoA-I) is secreted primarily by hepatocytes and plays an essential role in reverse cholesterol transport. Our previous studies revealed that apoA-I can mitigate the progression of metabolic dysfunction-associated steatohepatitis (MASH). However, there is no clear evidence to explain the relationship between apoA-I and IR. Here, we investigated the effects of apoA-I overexpression on IR in both HepG2 cells and mice. In vitro experiment results revealed that apoA-I overexpression can promote cellular glucose uptake in oleic acid-induced IR in HepG2 cells. High-fat, high-cholesterol, and high-fructose diets were used to induce IR in mice. The results showed that apoA-I overexpression improved glucose tolerance, reduced serum insulin levels, and ameliorated IR in diet-induced MASLD mice. Moreover, apoA-I promoted the expression of peroxisome proliferator-activated receptor α (PPARα) in the nucleus both in vitro and in vivo. In conclusion, apoA-I could alleviate MASLD by reducing IR in mice and might exert this effect through the PPARα pathway. Full article
(This article belongs to the Special Issue Apolipoproteins and Lipoproteins in Health and Disease, 3rd Edition)
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11 pages, 2246 KiB  
Article
Phenotype in Individuals with Heterozygous Rare Variants in LIPC Encoding Hepatic Lipase
by Erin O. Jacob, Jian Wang, Adam D. McIntyre and Robert A. Hegele
Int. J. Mol. Sci. 2024, 25(21), 11445; https://doi.org/10.3390/ijms252111445 - 24 Oct 2024
Viewed by 999
Abstract
Hepatic lipase deficiency is a rare genetic condition caused by biallelic loss-of-function variants in the LIPC gene encoding hepatic lipase. These variants reduce or abolish the protein’s lipolytic activity, resulting in elevated plasma lipids. The condition is classified as autosomal recessive, since dyslipidemia [...] Read more.
Hepatic lipase deficiency is a rare genetic condition caused by biallelic loss-of-function variants in the LIPC gene encoding hepatic lipase. These variants reduce or abolish the protein’s lipolytic activity, resulting in elevated plasma lipids. The condition is classified as autosomal recessive, since dyslipidemia is inconsistently observed in heterozygous patients with only one LIPC variant. However, this has been concluded from historical studies encompassing a few families and having very small sample sizes. Here, we conduct a retrospective chart review of 46 heterozygous subjects, each harboring one rare pathogenic LIPC variant. We compare plasma levels of total cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglycerides, and apolipoprotein B to those of matched controls without LIPC variants. Variant pathogenicity is classified according to the guidelines of the American College of Medical Genetics and Genomics. We observe that levels of total cholesterol, LDL-C, and triglycerides are significantly elevated in the LIPC variant heterozygotes, but HDL-C and apolipoprotein B are not. When filtering solely with respect to pathogenic or likely pathogenic variants, all lipid variables emerge as significantly elevated compared to controls. Thus, hepatic lipase deficiency may not necessarily be a recessive condition, but perhaps semi-dominant since individuals with one variant are phenotypically distinct from the controls. These hypothesis-generating findings regarding LIPC genetic variations observed in a clinical cohort should be evaluated in larger populations and databases. Full article
(This article belongs to the Special Issue Apolipoproteins and Lipoproteins in Health and Disease, 3rd Edition)
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13 pages, 804 KiB  
Article
Influence of Common Gene Variants on Lipid Levels and Risk of Coronary Heart Disease in Afro-Caribbeans
by Laurent Larifla, Valerie Bassien-Capsa, Fritz-Line Velayoudom, Vaneva Chingan-Martino, Yaovi Afassinou, Yann Ancedy, Olivier Galantine, Valérie Galantine, Livy Nicolas, Frédérique Martino, Patrick Numeric, Lydia Foucan and Steve E. Humphries
Int. J. Mol. Sci. 2024, 25(20), 11140; https://doi.org/10.3390/ijms252011140 - 17 Oct 2024
Viewed by 981
Abstract
A lower mortality rate from coronary artery disease (CAD) and a more favourable lipid profile have been reported in Afro-Caribbeans compared with people of European ancestry. The aim of this study was to determine whether common lipid variants identified in other populations are [...] Read more.
A lower mortality rate from coronary artery disease (CAD) and a more favourable lipid profile have been reported in Afro-Caribbeans compared with people of European ancestry. The aim of this study was to determine whether common lipid variants identified in other populations are associated with lipid levels and CAD in Afro-Caribbeans. We studied 705 Afro-Caribbeans (192 with CAD) who were genotyped for 13 lipid-associated variants. We calculated three polygenic risk scores (PRSs) for elevated LDL (LDL-PRS), decreased HDL (HDL-PRS), and elevated triglycerides (TG-PRS). LDL-PRS, HDL-PRS, and TG-PRS were associated with LDL, HDL, and TG levels, respectively. The LDL-PRS was positively associated with LDL > 2.6 mmol/L and with LDL > 3.0 mmol/L with ORs (odds ratios) of 1.33 (95% confidence interval (CI) = 1.14–1.56) and 1.40 (CI = 1.21–1.62), respectively. The HDL-PRS was associated with a low HDL category (HDL < 1.03 mmol/L) with an OR of 1.3 (CI = 1.04–1.63) and inversely associated with a high HDL category (HDL > 1.55 mmol/L) with an OR of 0.79 (CI = 0.65–0.96). The LDL-PRS was positively associated with CAD after adjustment for age, gender, hypertension, diabetes, and smoking with an OR of 1.27 (CI = 1.06–1.51) but not the HDL-PRS nor the TG-PRS. Results of the present study indicate that common lipid variants are associated with lipid levels and prevalent CAD in Afro-Caribbeans. Full article
(This article belongs to the Special Issue Apolipoproteins and Lipoproteins in Health and Disease, 3rd Edition)
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19 pages, 1704 KiB  
Article
Readdressing the Localization of Apolipoprotein E (APOE) in Mitochondria-Associated Endoplasmic Reticulum (ER) Membranes (MAMs): An Investigation of the Hepatic Protein–Protein Interactions of APOE with the Mitochondrial Proteins Lon Protease (LONP1), Mitochondrial Import Receptor Subunit TOM40 (TOMM40) and Voltage-Dependent Anion-Selective Channel 1 (VDAC1)
by Johanna Rueter, Gerald Rimbach, Stephanie Bilke, Andreas Tholey and Patricia Huebbe
Int. J. Mol. Sci. 2024, 25(19), 10597; https://doi.org/10.3390/ijms251910597 - 1 Oct 2024
Cited by 1 | Viewed by 1998
Abstract
As a component of circulating lipoproteins, APOE binds to cell surface receptors mediating lipoprotein metabolism and cholesterol transport. A growing body of evidence, including the identification of a broad variety of cellular proteins interacting with APOE, suggests additional independent functions. Investigating cellular localization [...] Read more.
As a component of circulating lipoproteins, APOE binds to cell surface receptors mediating lipoprotein metabolism and cholesterol transport. A growing body of evidence, including the identification of a broad variety of cellular proteins interacting with APOE, suggests additional independent functions. Investigating cellular localization and protein–protein interactions in cultured human hepatocytes, we aimed to contribute to the elucidation of hitherto unnoted cellular functions of APOE. We observed a strong accumulation of APOE in MAMs, equally evident for the two major isoforms APOE3 and APOE4. Using mass spectrometry proteome analyses, novel and previously noted APOE interactors were identified, including the mitochondrial proteins TOMM40, LONP1 and VDAC1. All three interactors were present in MAM fractions, which we think initially facilitates interactions with APOE. LONP1 is a protease with chaperone activity, which migrated to MAMs in response to ER stress, displaying a reinforced interaction with APOE. We therefore hypothesize that APOE may help in the unfolded protein response (UPR) by acting as a co-chaperone in cooperation with LONP1 at the interface of mitochondria and ER membranes. The interaction of APOE with the integral proteins TOMM40 and VDAC1 may point to the formation of bridging complexes connecting mitochondria with other organelles. Full article
(This article belongs to the Special Issue Apolipoproteins and Lipoproteins in Health and Disease, 3rd Edition)
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