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

Deadline for manuscript submissions: closed (20 April 2023) | Viewed by 40826

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Dr. Melania Gaggini

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Istituto di Fisiologia Clinica, National Research Council of Italy, Via Moruzzi 1, I-56124 Pisa, Italy
Interests: metabolic disease; organ pathophysiology; cardiovascular disease; metabolomic ad lipidomic technology
Special Issues, Collections and Topics in MDPI journals

Dr. Cristina Vassalle

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Guest Editor

Fondazione CNR-Regione Toscana G. Monasterio, Via Moruzzi 1, I-56124 Pisa, Italy
Interests: medicine; biochemistry; genetics and molecular biology cardiovascular disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiometabolic diseases are one of principal causes of death around the world. Lipids are the regulators of the biological processes that are associated with normal cell function, metabolism, and distribution. Abnormal lipid profile and changes in lipid components can have profound effects on cell function, the immune system, antioxidant defences, and inflammatory responses. The advent new tools and information technologies have made it feasible to analyse entire lipid profiles (lipidomics) in biofluids and tissues. The determination of individual lipid characteristics (composition and abundance) in biosamples could be a powerful tool that can be used to understand the mechanisms of lipid-based diseases. The mechanisms that link lipid metabolism and coronary artery diseases have been studied, but which lipids and particular species (i.e., ceramides, phosphocholine, lysophosphatidylcholines) are involved in this interaction remain poorly understood. We invite investigators to contribute either original research or review articles that are in accordance with this Special Issue, which focuses on the role and mechanisms of lipid dysregulation-related diseases, including obesity, diabetes, non-alcoholic fatty liver disease (NAFLD/NASH), atherosclerosis, hypertension, and coronary artery diseases. Subtopics that are also of interest include, but are not limited to, the following:

Insulin and glucose metabolism and cardiometabolic disease;
Lipid assessment and cardiometabolic syndrome;
Metabolomic/lipidomic approach and cardiometabolic risk;
Limits and advantages of the lipidomic techniques and translational opportunities towards a routinary clinical use;
Role of lipid-related biochemical and molecular markers as diagnostic/prognostic tools and therapeutic targets for cardiometabolic disease.

Dr. Melania Gaggini
Dr. Cristina Vassalle
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.

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Keywords

insulin resistance
dyslipidemia
obesity
diabetes
lipotoxicity
cardiovascular risk
lipidomic
cardiometabolic disease

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Published Papers (10 papers)

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Editorial

Jump to: Research, Review

3 pages, 206 KiB

Open AccessEditorial

Lipids Metabolism and Cardiometabolic Diseases

by Melania Gaggini and Cristina Vassalle

Int. J. Mol. Sci. 2023, 24(24), 17460; https://doi.org/10.3390/ijms242417460 - 14 Dec 2023

Viewed by 1102

Abstract

Cardiometabolic diseases (CMD) remains the major cause of morbidity and mortality in Western countries, with a marked increased in the last years [...] Full article

(This article belongs to the Special Issue Lipids Metabolism and Cardiometabolic Diseases)

Research

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12 pages, 623 KiB

Open AccessArticle

HDL Subclasses and the Distribution of Paraoxonase-1 Activity in Patients with ST-Segment Elevation Acute Myocardial Infarction

by Saska Djekic, Jelena Vekic, Aleksandra Zeljkovic, Jelena Kotur-Stevuljevic, Srdjan Kafedzic, Marija Zdravkovic, Ivan Ilic, Sasa Hinic, Milivoje Cerovic, Milica Stefanovic, Marija Mihajlovic, Aleksandar Neskovic and Natasa Bogavac-Stanojevic

Int. J. Mol. Sci. 2023, 24(11), 9384; https://doi.org/10.3390/ijms24119384 - 27 May 2023

Cited by 3 | Viewed by 1735

Abstract

The aim of this multicentric study was to assess the impacts of oxidative stress, inflammation, and the presence of small, dense, low-density lipoproteins (sdLDL) on the antioxidative function of high-density lipoprotein (HDL) subclasses and the distribution of paraoxonase-1 (PON1) activity within HDL in patients with ST-segment elevation acute myocardial infarction (STEMI). In 69 STEMI patients and 67 healthy control subjects, the lipoproteins’ subclasses were separated using polyacrylamide gradient (3–31%) gel electrophoresis. The relative proportion of sdLDL and each HDL subclass was evaluated by measuring the areas under the peaks of densitometric scans. The distribution of the relative proportion of PON1 activity within the HDL subclasses (pPON1 within HDL) was estimated using the zymogram method. The STEMI patients had significantly lower proportions of HDL2a and HDL3a subclasses (p = 0.001 and p < 0.001, respectively) and lower pPON1 within HDL3b (p = 0.006), as well as higher proportions of HDL3b and HDL3c subclasses (p = 0.013 and p < 0.001, respectively) and higher pPON1 within HDL2 than the controls. Independent positive associations between sdLDL and pPON1 within HDL3a and between malondialdehyde (MDA) and pPON1 within HDL2b were shown in the STEMI group. The increased oxidative stress and increased proportion of sdLDL in STEMI are closely related to the compromised antioxidative function of small HDL3 particles and the altered pPON1 within HDL. Full article

(This article belongs to the Special Issue Lipids Metabolism and Cardiometabolic Diseases)

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12 pages, 616 KiB

Open AccessArticle

Overexpression of microRNA-21-5p and microRNA-221-5p in Monocytes Increases the Risk of Developing Coronary Artery Disease

by Yazmín Estela Torres-Paz, Ricardo Gamboa, Giovanny Fuentevilla-Álvarez, María Elena Soto, Nadia González-Moyotl, Rocío Martínez-Alvarado, Margarita Torres-Tamayo, Edgar Samuel Ramírez-Marroquín, Xicoténcatl Vásquez-Jiménez, Víctor Sainz-Escarrega and Claudia Huesca-Gómez

Int. J. Mol. Sci. 2023, 24(10), 8641; https://doi.org/10.3390/ijms24108641 - 12 May 2023

Cited by 8 | Viewed by 1898

Abstract

MicroRNAs (miRs) regulate gene expression at the post-transcriptional level and are found to be present in monocytes. This study aimed to investigate miR-221-5p, miR-21-5p, and miR-155-5p, their expression in monocytes, and their role in coronary arterial disease (CAD). The study population comprised 110 subjects, and RT-qPCR was used to examine the miR-221-5p, miR-21-5p, and miR-155-5p expressions in monocytes. Results: the miR-21-5p (p = 0.001) and miR-221-5p (p < 0.001) expression levels were significantly higher in the CAD group, and the miR-155-5p (p = 0.021) expression levels were significantly lower in the CAD group; only miR-21-5p and miR-221-5p upregulation was found to be associated with an increased CAD risk. The results show significant increases in miR-21-5p in the unmedicated CAD group with the metformin patients vs. the healthy control group (p = 0.001) and vs. the medicated CAD group with metformin (p = 0.022). The same was true for miR-221-5p in the CAD patients unmedicated with metformin vs. the healthy control group (p < 0.001). Our results from Mexican CAD patients show that the overexpression in monocytes of miR-21-5p and miR-221-5p increases the risk of the development of CAD. In addition, in the CAD group, the metformin downregulated the expression of miR-21-5p and miR-221-5p. Also, the expression of endothelial nitric oxide synthase (NOS3) decreased significantly in our patients with CAD, regardless of whether they were medicated. Therefore, our findings allow for the proposal of new therapeutic strategies for the diagnosis and prognosis of CAD and the evaluation of treatment efficacy. Full article

(This article belongs to the Special Issue Lipids Metabolism and Cardiometabolic Diseases)

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14 pages, 1956 KiB

Open AccessArticle

CircRNA-PI4KB Induces Hepatic Lipid Deposition in Non-Alcoholic Fatty Liver Disease by Transporting miRNA-122 to Extra-Hepatocytes

by Chang-Hai Liu, Wei Jiang, Qingmin Zeng, Dongbo Wu, Hong Li, Lingyun Zhou, Lang Bai and Hong Tang

Int. J. Mol. Sci. 2023, 24(2), 1297; https://doi.org/10.3390/ijms24021297 - 9 Jan 2023

Cited by 4 | Viewed by 2093

Abstract

Ectopic fat deposition in the liver, known as non-alcoholic fatty liver disease (NAFLD), affects up to 30% of the worldwide population. miRNA-122, the most abundant liver-specific miRNA, protects hepatic steatosis and inhibits cholesterol and fatty acid synthesis in NAFLD. Previously, we have shown that compared with its expression in healthy controls, miRNA-122 decreased in the liver tissue but gradually increased in the serum of patients with non-alcoholic fatty liver disease and non-alcoholic steatohepatitis, suggesting that miRNA-122 could have been transported to the serum. Here, we aimed to confirm and unravel the mechanism of transportation of miRNA-122 to extra-hepatocytes. Our findings showed a decrease in the intra-hepatocyte miRNA-122 and an increase in the extra-hepatocyte (medium level) miRNA-122, suggesting the miRNA-122 “escaped” from the intra-hepatocyte due to an increased extra-hepatocyte excretion. Using bioinformatics tools, we showed that miRNA-122 binds to circPI4KB, which was further validated by an RNA pull-down and luciferase reporter assay. The levels of circPI4KB in intra- and extra-hepatocytes corresponded to that of miRNA-122, and the overexpression of circPI4KB increased the miRNA-122 in extra-hepatocytes, consequently accomplishing a decreased protective role of miRNA-122 in inhibiting the lipid deposition. The present study provides a new explanation for the pathogenesis of the hepatic lipid deposition in NAFLD. Full article

(This article belongs to the Special Issue Lipids Metabolism and Cardiometabolic Diseases)

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18 pages, 3551 KiB

Open AccessArticle

Treatment with EV-miRNAs Alleviates Obesity-Associated Metabolic Dysfunction in Mice

by Carlos Castaño, Aline Meza-Ramos, Montserrat Batlle, Eduard Guasch, Anna Novials and Marcelina Párrizas

Int. J. Mol. Sci. 2022, 23(23), 14920; https://doi.org/10.3390/ijms232314920 - 29 Nov 2022

Cited by 9 | Viewed by 2439

Abstract

Most cells release extracellular vesicles (EVs) that can be detected circulating in blood. We and others have shown that the microRNA contents of these vesicles induce transcriptomic changes in acceptor cells, contributing to the adjustment of metabolic homeostasis in response to environmental demands. Here, we explore the potential for modulating obesity- and exercise-derived EV-microRNAs to treat the metabolic dysfunction associated with obesity in mice. Treatment with EV-miRNAs alleviated glucose intolerance and insulin resistance in obese mice to an extent similar to that of high-intensity interval training, although only exercise improved cardiorespiratory fitness and decreased body weight. Mechanistically, EV-miRNAs decreased fatty acid and cholesterol biosynthesis pathways in the liver, reducing hepatic steatosis and increasing insulin sensitivity, resulting in decreased glycemia and triglyceridemia. Our data suggest that manipulation of EV-miRNAs may be a viable strategy to alleviate metabolic dysfunction in obese and diabetic patients who are unable to exercise, although actual physical activity is needed to improve cardiorespiratory fitness. Full article

(This article belongs to the Special Issue Lipids Metabolism and Cardiometabolic Diseases)

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20 pages, 4090 KiB

Open AccessArticle

Fatty Acid Amide Hydrolase Deficiency Is Associated with Deleterious Cardiac Effects after Myocardial Ischemia and Reperfusion in Mice

by Sanela Rajlic, Luise Surmann, Pia Zimmermann, Christina Katharina Weisheit, Laura Bindila, Hendrik Treede, Markus Velten, Andreas Daiber and Georg Daniel Duerr

Int. J. Mol. Sci. 2022, 23(20), 12690; https://doi.org/10.3390/ijms232012690 - 21 Oct 2022

Cited by 5 | Viewed by 2314

Abstract

Ischemic cardiomyopathy leads to inflammation and left ventricular (LV) dysfunction. Animal studies provided evidence for cardioprotective effects of the endocannabinoid system, including cardiomyocyte adaptation, inflammation, and remodeling. Cannabinoid type-2 receptor (CB2) deficiency led to increased apoptosis and infarctions with worsened LV function in ischemic cardiomyopathy. The aim of our study was to investigate a possible cardioprotective effect of endocannabinoid anandamide (AEA) after ischemia and reperfusion (I/R). Therefore, fatty acid amide hydrolase deficient (FAAH)^−/− mice were subjected to repetitive, daily, 15 min, left anterior descending artery (LAD) occlusion over 3 and 7 consecutive days. Interestingly, FAAH^−/− mice showed stigmata such as enhanced inflammation, cardiomyocyte loss, stronger remodeling, and persistent scar with deteriorated LV function compared to wild-type (WT) littermates. As endocannabinoids also activate PPAR-α (peroxisome proliferator-activated receptor), PPAR-α mediated effects of AEA were eliminated with PPAR-α antagonist GW6471 i.v. in FAAH^−/− mice. LV function was assessed using M-mode echocardiography. Immunohistochemical analysis revealed apoptosis, macrophage accumulation, collagen deposition, and remodeling. Hypertrophy was determined by cardiomyocyte area and heart weight/tibia length. Molecular analyses involved Taqman^® RT-qPCR and immune cells were analyzed with fluorescence-activated cell sorting (FACS). Most importantly, collagen deposition was reduced to WT levels when FAAH^−/− mice were treated with GW6471. Chemokine ligand-2 (CCL2) expression was significantly higher in FAAH^−/− mice compared to WT, followed by higher macrophage infiltration in infarcted areas, both being reversed by GW6471 treatment. Besides restoring antioxidative properties and contractile elements, PPAR-α antagonism also reversed hypertrophy and remodeling in FAAH^−/− mice. Finally, FAAH^−/−-mice showed more substantial downregulation of PPAR-α compared to WT, suggesting a compensatory mechanism as endocannabinoids are also ligands for PPAR-α, and its activation causes lipotoxicity leading to cardiomyocyte apoptosis. Our study gives novel insights into the role of endocannabinoids acting via PPAR-α. We hypothesize that the increase in endocannabinoids may have partially detrimental effects on cardiomyocyte survival due to PPAR-α activation. Full article

(This article belongs to the Special Issue Lipids Metabolism and Cardiometabolic Diseases)

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12 pages, 2237 KiB

Open AccessArticle

Molecular Characterization of Plasma HDL, LDL, and VLDL Lipids Cargos from Atherosclerotic Patients with Advanced Carotid Lesions: A Preliminary Report

by Gabriele Nieddu, Elena Michelucci, Marilena Formato, Cristina Ciampelli, Gabriele Obino, Giovanni Signore, Nicoletta Di Giorgi, Silvia Rocchiccioli and Antonio Junior Lepedda

Int. J. Mol. Sci. 2022, 23(20), 12449; https://doi.org/10.3390/ijms232012449 - 18 Oct 2022

Cited by 9 | Viewed by 2483

Abstract

Carotid atherosclerosis represents a relevant healthcare problem, since unstable plaques are responsible for approximately 15% of neurologic events, namely transient ischemic attack and stroke. Although statins treatment has proven effective in reducing LDL-cholesterol and the onset of acute clinical events, a residual risk may persist suggesting the need for the detection of reliable molecular markers useful for the identification of patients at higher risk regardless of optimal medical therapy. In this regard, several lines of evidence show a relationship among specific biologically active plasma lipids, atherosclerosis, and acute clinical events. We performed a Selected Reaction Monitoring-based High Performance Liquid Chromatography-tandem Mass Spectrometry (SRM-based HPLC-MS/MS) analysis on plasma HDL, LDL, and VLDL fractions purified, by isopycnic salt gradient ultracentrifugation, from twenty-eight patients undergoing carotid endarterectomy, having either a “hard” or a “soft” plaque, with the aim of characterizing the specific lipidomic patterns associated with features of carotid plaque instability. One hundred and thirty lipid species encompassing different lipid (sub)classes were monitored. Supervised multivariate analysis showed that lipids belonging to phosphatidylethanolamine (PE), sphingomyelin (SM), and diacylglycerol (DG) classes mostly contribute to discrimination within each lipoprotein fraction according to the plaque typology. Differential analysis evidenced a significant dysregulation of LDL PE (38:6), SM (32:1), and SM (32:2) between the two groups of patients (adj. p-value threshold = 0.05 and log₂FC ≥ |0.58|). Using this approach, some LDL-associated markers of plaque vulnerability have been identified, in line with the current knowledge of the key roles of these phospholipids in lipoprotein metabolism and cardiovascular disease. This proof-of-concept study reports promising results, showing that lipoprotein lipidomics may present a valuable approach for identifying new biomarkers of potential clinical relevance. Full article

(This article belongs to the Special Issue Lipids Metabolism and Cardiometabolic Diseases)

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20 pages, 4391 KiB

Open AccessArticle

Lipidomic Approaches to Study HDL Metabolism in Patients with Central Obesity Diagnosed with Metabolic Syndrome

by Gabriele Mocciaro, Simona D’Amore, Benjamin Jenkins, Richard Kay, Antonio Murgia, Luis Vicente Herrera-Marcos, Stefanie Neun, Alice P. Sowton, Zoe Hall, Susana Alejandra Palma-Duran, Giuseppe Palasciano, Frank Reimann, Andrew Murray, Patrizia Suppressa, Carlo Sabbà, Antonio Moschetta, Albert Koulman, Julian L. Griffin and Michele Vacca

Int. J. Mol. Sci. 2022, 23(12), 6786; https://doi.org/10.3390/ijms23126786 - 17 Jun 2022

Cited by 22 | Viewed by 3947

Abstract

The metabolic syndrome (MetS) is a cluster of cardiovascular risk factors characterised by central obesity, atherogenic dyslipidaemia, and changes in the circulating lipidome; the underlying mechanisms that lead to this lipid remodelling have only been partially elucidated. This study used an integrated “omics” approach (untargeted whole serum lipidomics, targeted proteomics, and lipoprotein lipidomics) to study lipoprotein remodelling and HDL composition in subjects with central obesity diagnosed with MetS (vs. controls). Compared with healthy subjects, MetS patients showed higher free fatty acids, diglycerides, phosphatidylcholines, and triglycerides, particularly those enriched in products of de novo lipogenesis. On the other hand, the “lysophosphatidylcholines to phosphatidylcholines” and “cholesteryl ester to free cholesterol” ratios were reduced, pointing to a lower activity of lecithin cholesterol acyltransferase (LCAT) in MetS; LCAT activity (directly measured and predicted by lipidomic ratios) was positively correlated with high-density lipoprotein cholesterol (HDL-C) and negatively correlated with body mass index (BMI) and insulin resistance. Moreover, many phosphatidylcholines and sphingomyelins were significantly lower in the HDL of MetS patients and strongly correlated with BMI and clinical metabolic parameters. These results suggest that MetS is associated with an impairment of phospholipid metabolism in HDL, partially led by LCAT, and associated with obesity and underlying insulin resistance. This study proposes a candidate strategy to use integrated “omics” approaches to gain mechanistic insights into lipoprotein remodelling, thus deepening the knowledge regarding the molecular basis of the association between MetS and atherosclerosis. Full article

(This article belongs to the Special Issue Lipids Metabolism and Cardiometabolic Diseases)

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Review

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18 pages, 1322 KiB

Open AccessReview

Lipids in Atherosclerosis: Pathophysiology and the Role of Calculated Lipid Indices in Assessing Cardiovascular Risk in Patients with Hyperlipidemia

by Melania Gaggini, Francesca Gorini and Cristina Vassalle

Int. J. Mol. Sci. 2023, 24(1), 75; https://doi.org/10.3390/ijms24010075 - 21 Dec 2022

Cited by 41 | Viewed by 9090

Abstract

The role of lipids is essential in any phase of the atherosclerotic process, which is considered a chronic lipid-related and inflammatory condition. The traditional lipid profile (including the evaluation of total cholesterol, triglycerides, high-density lipoprotein, and low-density lipoprotein) is a well-established tool to assess the risk of atherosclerosis and as such has been widely used as a pillar of cardiovascular disease prevention and as a target of pharmacological treatments in clinical practice over the last decades. However, other non-traditional lipids have emerged as possible alternative predictors of cardiometabolic risk in addition to traditional single or panel lipids, as they better reflect the overall interaction between lipid/lipoprotein fractions. Therefore, this review deals with the lipid involvement characterizing the pathophysiology of atherosclerosis, discussing some recently proposed non-traditional lipid indices and, in the light of available knowledge, their actual potential as new additive tools to better stratify cardiovascular risk in patients with hyperlipidemia as well as possible therapeutic targets in the clinical practice. Full article

(This article belongs to the Special Issue Lipids Metabolism and Cardiometabolic Diseases)

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9 pages, 276 KiB

Open AccessReview

Importance of Coagulation Factors as Critical Components of Premature Cardiovascular Disease in Familial Hypercholesterolemia

by Uffe Ravnskov, Michel de Lorgeril, Malcolm Kendrick and David M. Diamond

Int. J. Mol. Sci. 2022, 23(16), 9146; https://doi.org/10.3390/ijms23169146 - 15 Aug 2022

Cited by 7 | Viewed by 12438

Abstract

For almost a century, familial hypercholesterolemia (FH) has been considered a serious disease, causing atherosclerosis, cardiovascular disease, and ischemic stroke. Closely related to this is the widespread acceptance that its cause is greatly increased low-density-lipoprotein cholesterol (LDL-C). However, numerous observations and experiments in this field are in conflict with Bradford Hill’s criteria for causality. For instance, those with FH demonstrate no association between LDL-C and the degree of atherosclerosis; coronary artery calcium (CAC) shows no or an inverse association with LDL-C, and on average, the life span of those with FH is about the same as the surrounding population. Furthermore, no controlled, randomized cholesterol-lowering trial restricted to those with FH has demonstrated a positive outcome. On the other hand, a number of studies suggest that increased thrombogenic factors—either procoagulant or those that lead to high platelet reactivity—may be the primary risk factors in FH. Those individuals who die prematurely have either higher lipoprotein (a) (Lp(a)), higher factor VIII and/or higher fibrinogen compared with those with a normal lifespan, whereas their LDL-C does not differ. Conclusions: Many observational and experimental studies have demonstrated that high LDL-C cannot be the cause of premature cardiovascular mortality among people with FH. The number who die early is also much smaller than expected. Apparently, some individuals with FH may have inherited other, more important risk factors than a high LDL-C. In accordance with this, our review has shown that increased coagulation factors are the commonest cause, but there may be other ones as well. Full article

(This article belongs to the Special Issue Lipids Metabolism and Cardiometabolic Diseases)

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