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Molecular Studies of Lipid Metabolism-Related Diseases
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Molecular Studies of Lipid Metabolism-Related Diseases

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Biochemistry, Molecular and Cellular Biology".

Deadline for manuscript submissions: closed (31 January 2024) | Viewed by 3353

Special Issue Editor

Prof. Dr. Jui-Hung Yen

E-Mail Website
Guest Editor
Department of Molecular Biology and Human Genetics, Tzu Chi University, Hualien 97004, Taiwan
Interests: phytochemicals; food chemistry; lipid metabolism; leukemia; neuroprotection
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The dysregulation of lipid metabolism is not only associated with atherosclerotic cardiovascular disorders (ASCVDs) but also other diseases, such as obesity, type 2 diabetes, metabolic syndrome, non-alcoholic fatty liver disease (NAFLD), neurodegenerative diseases, viral hepatitis, and cancers. Dyslipidemia is characterized by aberrant levels of cholesterol, low-density lipoprotein cholesterol (LDL-C), triglycerides (TGs), TG-rich lipoproteins (TGRLs), and HDL in plasma. The precise regulation or targeting of genes involved in dyslipidemia, such as HMGCR, LDLR, PCSK9, APOB, APOC, Lp(a), CETP, ANGPTL3, and ACLY, is an emerging approach for the prevention and treatment of ASCVDs as well as other chronic diseases with lipid dysregulation. The modulation of plasma lipid homeostasis may be achieved through diet, lifestyle changes, or the use of pharmacological interventions for lipid-metabolism-related genes. In this Special Issue, we invite paper submissions of research into the molecular effects of genes, signaling pathways, therapeutic agents, and intervention strategies for the management of lipid dysregulation in the prevention or treatment of lipid-metabolism-related diseases. Original articles and reviews are welcome.

Prof. Dr. Jui-Hung Yen
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. Current Issues in Molecular Biology 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 2200 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

  • lipid metabolism
  • ASCVDs
  • obesity
  • NAFLD
  • dyslipidemia
  • LDL-C
  • TG
  • lipoproteins

Published Papers (2 papers)

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14 pages, 1347 KiB  
Article
Constructing Lipoparticles Capable of Endothelial Cell-Derived Exosome-Mediated Delivery of Anti-miR-33a-5p to Cultured Macrophages
by Jing Echesabal-Chen, Kun Huang, Lucia Vojtech, Olanrewaju Oladosu, Ikechukwu Esobi, Rakesh Sachdeva, Naren Vyavahare, Hanjoong Jo and Alexis Stamatikos
Curr. Issues Mol. Biol. 2023, 45(7), 5631-5644; https://doi.org/10.3390/cimb45070355 - 4 Jul 2023
Cited by 1 | Viewed by 2129
Abstract
Atherosclerosis is driven by intimal arterial macrophages accumulating cholesterol. Atherosclerosis also predominantly occurs in areas consisting of proinflammatory arterial endothelial cells. At time of writing, there are no available clinical treatments that precisely remove excess cholesterol from lipid-laden intimal arterial macrophages. Delivery of [...] Read more.
Atherosclerosis is driven by intimal arterial macrophages accumulating cholesterol. Atherosclerosis also predominantly occurs in areas consisting of proinflammatory arterial endothelial cells. At time of writing, there are no available clinical treatments that precisely remove excess cholesterol from lipid-laden intimal arterial macrophages. Delivery of anti-miR-33a-5p to macrophages has been shown to increase apoAI-mediated cholesterol efflux via ABCA1 upregulation but delivering transgenes to intimal arterial macrophages is challenging due to endothelial cell barrier integrity. In this study, we aimed to test whether lipoparticles targeting proinflammatory endothelial cells can participate in endothelial cell-derived exosome exploitation to facilitate exosome-mediated transgene delivery to macrophages. We constructed lipoparticles that precisely target the proinflammatory endothelium and contain a plasmid that expresses XMOTIF-tagged anti-miR-33a-5p (LP-pXMoAntimiR33a5p), as XMOTIF-tagged small RNA demonstrates the capacity to be selectively shuttled into exosomes. The cultured cells used in our study were immortalized mouse aortic endothelial cells (iMAECs) and RAW 264.7 macrophages. From our results, we observed a significant decrease in miR-33a-5p expression in macrophages treated with exosomes released basolaterally by LPS-challenged iMAECs incubated with LP-pXMoAntimiR33a5p when compared to control macrophages. This decrease in miR-33a-5p expression in the treated macrophages caused ABCA1 upregulation as determined by a significant increase in ABCA1 protein expression in the treated macrophages when compared to the macrophage control group. The increase in ABCA1 protein also simulated ABCA1-dependent cholesterol efflux in treated macrophages—as we observed a significant increase in apoAI-mediated cholesterol efflux—when compared to the control group of macrophages. Based on these findings, strategies that involve combining proinflammatory-targeting lipoparticles and exploitation of endothelial cell-derived exosomes appear to be promising approaches for delivering atheroprotective transgenes to lipid-laden arterial intimal macrophages. Full article
(This article belongs to the Special Issue Molecular Studies of Lipid Metabolism-Related Diseases)
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11 pages, 968 KiB  
Brief Report
Effects of Chronic Sleep Restriction on Transcriptional Sirtuin 1 Signaling Regulation in Male Mice White Adipose Tissue
by Marco Rendine, Paolo Cocci, Luisa de Vivo, Michele Bellesi and Francesco Alessandro Palermo
Curr. Issues Mol. Biol. 2024, 46(3), 2144-2154; https://doi.org/10.3390/cimb46030138 - 7 Mar 2024
Viewed by 836
Abstract
Chronic sleep restriction (CSR) is a prevalent issue in modern society that is associated with several pathological states, ranging from neuropsychiatric to metabolic diseases. Despite its known impact on metabolism, the specific effects of CSR on the molecular mechanisms involved in maintaining metabolic [...] Read more.
Chronic sleep restriction (CSR) is a prevalent issue in modern society that is associated with several pathological states, ranging from neuropsychiatric to metabolic diseases. Despite its known impact on metabolism, the specific effects of CSR on the molecular mechanisms involved in maintaining metabolic homeostasis at the level of white adipose tissue (WAT) remain poorly understood. Therefore, this study aimed to investigate the influence of CSR on sirtuin 1 (SIRT1) and the peroxisome proliferator-activated receptor γ (PPARγ) signaling pathway in the WAT of young male mice. Both genes interact with specific targets involved in multiple metabolic processes, including adipocyte differentiation, browning, and lipid metabolism. The quantitative PCR (qPCR) results demonstrated a significant upregulation of SIRT-1 and some of its target genes associated with the transcriptional regulation of lipid homeostasis (i.e., PPARα, PPARγ, PGC-1α, and SREBF) and adipose tissue development (i.e., leptin, adiponectin) in CSR mice. On the contrary, DNA-binding transcription factors (i.e., CEBP-β and C-myc), which play a pivotal function during the adipogenesis process, were found to be down-regulated. Our results also suggest that the induction of SIRT1-dependent molecular pathways prevents weight gain. Overall, these findings offer new, valuable insights into the molecular adaptations of WAT to CSR, in order to support increased energy demand due to sleep loss. Full article
(This article belongs to the Special Issue Molecular Studies of Lipid Metabolism-Related Diseases)
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