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Lipid Metabolism and Signaling in Tumors and Cerebrovascular Diseases 2.0
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Lipid Metabolism and Signaling in Tumors and Cerebrovascular Diseases 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: 30 April 2024 | Viewed by 8260

Special Issue Editors

Dr. Laura Gatti

E-Mail Website
Guest Editor
Neurobiology Laboratory, Fondazione IRCCS Istituto Neurologico Carlo Besta, 20133 Milan, Italy
Interests: cerebrovascular diseases; angiogenesis; antitumor agents; platinum compounds; antitumor drug resistance; apoptosis; liquid biopsy; ovarian cancer treatment; unfolded protein response; proteasome pathway; lipid metabolism
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Riccardo Ghidoni

E-Mail Website
Guest Editor
Department of Health Sciences, University of Milan, 20142 Milan, Italy
Interests: polyphenols; cancer; bioactive lipids
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is the continuation of our 2021 Special Issue “Lipid Metabolism and Signaling in Tumors and Cerebrovascular Diseases”.

Lipid molecules have been reported to regulate a broad range of cellular functions, from cell signaling and membrane dynamics to intercellular communication and gene expression.

A large body of evidence supports that alterations of lipid metabolism may be implicated in the development of cancer. The deregulation of lipid metabolism occurs in tumors as a result of the activation of oncogenic pathways. Cerebrovascular diseases that considerably threaten brain health are likely to be associated with lipid deregulation. Thus, knowledge regarding lipid homeostasis represents a powerful tool providing another layer of details at the molecular and cellular levels that may help in the exploration of novel biomarkers and new options for the treatment of such diseases.

The aim of this Special Issue is to update readers regarding state-of-the-art research into lipid metabolism and signaling in tumors and cerebrovascular diseases.

Authors are invited to submit original research and review articles. Topics include, but are not limited to:

  • Bioactive lipids in cell signaling.
  • Lipid molecules as therapeutic targets and pharmacological agents.
  • Lipids as diagnostic and prognostic biomarkers of disease.
  • Lipids in metabolic networks.
  • New advances in lipid analysis and lipidomics.

Dr. Laura Gatti
Prof. Dr. Riccardo Ghidoni
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

  • lipids
  • sphingolipids
  • phospholipids
  • cholesterol
  • fatty acids
  • solid tumors
  • hematological tumors
  • cerebrovascular diseases

Published Papers (4 papers)

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Review

35 pages, 2685 KiB  
Review
Lipoprotein(a) and Atherosclerotic Cardiovascular Disease: Where Do We Stand?
by Georgios Tsioulos, Dimitris Kounatidis, Natalia G. Vallianou, Aikaterini Poulaki, Evangelia Kotsi, Gerasimos Socrates Christodoulatos, Dimitrios Tsilingiris, Irene Karampela, Alexandros Skourtis and Maria Dalamaga
Int. J. Mol. Sci. 2024, 25(6), 3537; https://doi.org/10.3390/ijms25063537 - 21 Mar 2024
Viewed by 844
Abstract
Lipoprotein(a) [Lp(a)] consists of a low-density lipoprotein-like molecule and an apolipoprotein(a) [apo(a)] particle. Lp(a) has been suggested to be an independent risk factor of atherosclerotic cardiovascular disease (ASCVD). Lp(a) plasma levels are considered to be 70–90% genetically determined through the codominant expression of [...] Read more.
Lipoprotein(a) [Lp(a)] consists of a low-density lipoprotein-like molecule and an apolipoprotein(a) [apo(a)] particle. Lp(a) has been suggested to be an independent risk factor of atherosclerotic cardiovascular disease (ASCVD). Lp(a) plasma levels are considered to be 70–90% genetically determined through the codominant expression of the LPA gene. Therefore, Lp(a) levels are almost stable during an individual’s lifetime. This lifelong stability, together with the difficulties in measuring Lp(a) levels in a standardized manner, may account for the scarcity of available drugs targeting Lp(a). In this review, we synopsize the latest data regarding the structure, metabolism, and factors affecting circulating levels of Lp(a), as well as the laboratory determination measurement of Lp(a), its role in the pathogenesis of ASCVD and thrombosis, and the potential use of various therapeutic agents targeting Lp(a). In particular, we discuss novel agents, such as antisense oligonucleotides (ASOs) and small interfering RNAs (siRNAs) that are currently being developed and target Lp(a). The promising role of muvalaplin, an oral inhibitor of Lp(a) formation, is then further analyzed. Full article
(This article belongs to the Special Issue Lipid Metabolism and Signaling in Tumors and Cerebrovascular Diseases 2.0)
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15 pages, 568 KiB  
Review
Lipidomic Approaches in Common and Rare Cerebrovascular Diseases: The Discovery of Unconventional Lipids as Novel Biomarkers
by Antonella Potenza, Gemma Gorla, Tatiana Carrozzini, Anna Bersano, Laura Gatti and Giuliana Pollaci
Int. J. Mol. Sci. 2023, 24(16), 12744; https://doi.org/10.3390/ijms241612744 - 13 Aug 2023
Viewed by 1066
Abstract
Stroke remains a major cause of death and disability worldwide. Identifying new circulating biomarkers able to distinguish and monitor common and rare cerebrovascular diseases that lead to stroke is of great importance. Biomarkers provide complementary information that may improve diagnosis, prognosis and prediction [...] Read more.
Stroke remains a major cause of death and disability worldwide. Identifying new circulating biomarkers able to distinguish and monitor common and rare cerebrovascular diseases that lead to stroke is of great importance. Biomarkers provide complementary information that may improve diagnosis, prognosis and prediction of progression as well. Furthermore, biomarkers can contribute to filling the gap in knowledge concerning the underlying disease mechanisms by pointing out novel potential therapeutic targets for personalized medicine. If many “conventional” lipid biomarkers are already known to exert a relevant role in cerebrovascular diseases, the aim of our study is to review novel “unconventional” lipid biomarkers that have been recently identified in common and rare cerebrovascular disorders using novel, cutting-edge lipidomic approaches. Full article
(This article belongs to the Special Issue Lipid Metabolism and Signaling in Tumors and Cerebrovascular Diseases 2.0)
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10 pages, 738 KiB  
Review
Genotype and Phenotype Differences in CADASIL from an Asian Perspective
by Yerim Kim, Jong Seok Bae, Ju-Young Lee, Hong Ki Song, Ju-Hun Lee, Minwoo Lee, Chulho Kim and Sang-Hwa Lee
Int. J. Mol. Sci. 2022, 23(19), 11506; https://doi.org/10.3390/ijms231911506 - 29 Sep 2022
Cited by 8 | Viewed by 2248
Abstract
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a hereditary cerebral small-vessel disease caused by mutations in the NOTCH3 gene. Classical pathogenic mechanisms are associated with cysteine gain or loss, but recent studies suggest that cysteine-sparing mutations might have a [...] Read more.
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a hereditary cerebral small-vessel disease caused by mutations in the NOTCH3 gene. Classical pathogenic mechanisms are associated with cysteine gain or loss, but recent studies suggest that cysteine-sparing mutations might have a potential role as a pathogen. In comparison with CADASIL patients in Western countries, there are several differences in Asian patients: (1) prevalent locus of NOTCH3 mutations (exons 2–6 [particularly exon 4] vs. exon 11), (2) age at symptom onset, (3) prevalence of cerebral microbleeds and hemorrhagic stroke, (4) clinical symptoms, and (5) severity of white matter hyperintensities and typical involvement of the anterior temporal pole in magnetic resonance imaging. Both ethnicity and founder effects contribute to these differences in the clinical NOTCH3 spectrum in different cohorts. More functional investigations from diverse races are needed to clarify unknown but novel variants of NOTCH3 mutations. This review may broaden the spectrum of NOTCH3 variants from an Asian perspective and draw attention to the hidden pathogenic roles of NOTCH3 variants. Full article
(This article belongs to the Special Issue Lipid Metabolism and Signaling in Tumors and Cerebrovascular Diseases 2.0)
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14 pages, 1614 KiB  
Review
Novel Multifaceted Roles for RNF213 Protein
by Giuliana Pollaci, Gemma Gorla, Antonella Potenza, Tatiana Carrozzini, Isabella Canavero, Anna Bersano and Laura Gatti
Int. J. Mol. Sci. 2022, 23(9), 4492; https://doi.org/10.3390/ijms23094492 - 19 Apr 2022
Cited by 19 | Viewed by 3352
Abstract
Ring Finger Protein 213 (RNF213), also known as Mysterin, is the major susceptibility factor for Moyamoya Arteriopathy (MA), a progressive cerebrovascular disorder that often leads to brain stroke in adults and children. Although several rare RNF213 polymorphisms have been reported, no major susceptibility [...] Read more.
Ring Finger Protein 213 (RNF213), also known as Mysterin, is the major susceptibility factor for Moyamoya Arteriopathy (MA), a progressive cerebrovascular disorder that often leads to brain stroke in adults and children. Although several rare RNF213 polymorphisms have been reported, no major susceptibility variant has been identified to date in Caucasian patients, thus frustrating the attempts to identify putative therapeutic targets for MA treatment. For these reasons, the investigation of novel biochemical functions, substrates and unknown partners of RNF213 will help to unravel the pathogenic mechanisms of MA and will facilitate variant interpretations in a diagnostic context in the future. The aim of the present review is to discuss novel perspectives regarding emerging RNF213 roles in light of recent literature updates and dissect their relevance for understanding MA and for the design of future research studies. Since its identification, RNF213 involvement in angiogenesis and vasculogenesis has strengthened, together with its role in inflammatory signals and proliferation pathways. Most recent studies have been increasingly focused on its relevance in antimicrobial activity and lipid metabolism, highlighting new intriguing perspectives. The last area could suggest the main role of RNF213 in the proteasome pathway, thus reinforcing the hypotheses already previously formulated that depict the protein as an important regulator of the stability of client proteins involved in angiogenesis. We believe that the novel evidence reviewed here may contribute to untangling the complex and still obscure pathogenesis of MA that is reflected in the lack of therapies able to slow down or halt disease progression and severity. Full article
(This article belongs to the Special Issue Lipid Metabolism and Signaling in Tumors and Cerebrovascular Diseases 2.0)
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