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Molecular and Translational Research in Cardiovascular Endocrinology, Cardio-Metabolic Diseases and Non-Alcoholic Fatty Liver Disease (NAFLD): 2nd Edition

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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 July 2025 | Viewed by 9798

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Prof. Dr. Eva Kassi

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1. Department of Biochemistry, Medical School of Athens, National and Kapodistrian University of Athens, 11527 Athens, Greece
2. Unit of Endocrinology, First Department of Propaedeutic Internal Medicine, Laiko Hospital, National & Kapodistrian University of Athens, 11527 Athens, Greece
Interests: women’s health; cardiovascular endocrinology; atherosclerosis; non-alcoholic fatty liver disease; endocrinology of adrenals; oestrogen receptor signalling; glucocorticoid receptor signalling; clock system in benign diseases and malignancies; ICI (immune checkpoint inhibitor)-related endocrinopathies; neuroendocrine tumours; vitamin D; calcium and phosphate metabolic disorders; gynaecological cancers
Special Issues, Collections and Topics in MDPI journals

Dr. Ioannis Kyrou

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1. Warwick Medical School, University of Warwick, Coventry CV4 7AL, UK
2. Warwickshire Institute for the Study of Diabetes, Endocrinology and Metabolism (WISDEM), University Hospitals Coventry and Warwickshire NHS Trust, Coventry CV2 2DX, UK
3. Centre for Sport, Exercise and Life Sciences, Research Institute for Health & Wellbeing, Coventry University, Coventry CV1 5FB, UK
4. Aston Medical School, College of Health and Life Sciences, Aston University, Birmingham B4 7ET, UK
5. Laboratory of Dietetics and Quality of Life, Department of Food Science and Human Nutrition, School of Food and Nutritional Sciences, Agricultural University of Athens, 11855 Athens, Greece
Interests: metabolism and energy homeostasis; nutrition; cardiovascular endocrinology; cardiovascular disease and atherosclerosis; exercise and health; COVID 19; epidemiology of non-communicable diseases and public health; obesity and obesity-related complications; type 2 diabetes; non-alcoholic fatty liver disease (NAFLD); endocrinology; endocrine-disrupting chemicals; polycystic ovary syndrome (PCOS); mental-health stress and the HPA axis
Special Issues, Collections and Topics in MDPI journals

Dr. Harpal S. Randeva

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Dear Colleagues,

This Special Issue is a continuation of the first Special Issue “Molecular and Translational Research in Cardiovascular Endocrinology, Cardio-Metabolic Diseases and Non-Alcoholic Fatty Liver Disease (NAFLD)”.

Cardiovascular tissues have been recognized as dynamic endocrine organs, with vital stimuli that affect the cardiovascular system acting in an endocrine manner through hormone receptors. Many of these signaling systems are complex and so interconnected, that, in many cases, the interlinked components are hard to separate.

Thus, cardiovascular disease, endocrinology, diabetes and metabolism represent closely linked disciplines, giving rise to the field of cardiovascular endocrinology. Moreover, pituitary, adrenal, parathyroid, thyroid and gender hormone excesses or deficiencies, as well as glucose and lipid metabolism disorders, may further impact on cardiovascular disease risk (e.g., directly or indirectly through atherosclerosis, heart failure and non-alcoholic fatty liver disease, NAFLD).

Despite the important advances in the field of cardiovascular endocrinology through recent molecular and translational research, there are still open issues regarding the underlying pathogenetic mechanisms, as well as the exact effects/impact of various interventions/treatments, such as lifestyle modification interventions (e.g., dietary and exercise interventions) or pharmacological therapies (e.g., anti-hypertensive, lipid-lowering, anti-diabetic drugs , etc.), which may target more than one aspects/factors of cardiometabolic diseases.

This Special Issue, which is edited by Prof E. Kassi, As. Prof. I. Kyrou and Prof. H.S. Randeva with the aid of our Topical Advisory Panel Member Dr. Narjes Nasiri-Ansari (Department of Biochemistry, Medical School, National and Kapodistrian University of Athens, Greece), focuses on cardiometabolic diseases and endocrine-related cardiovascular diseases, including atherosclerosis, heart failure, arterial hypertension, metabolic syndrome, obesity, diabetes mellitus, chronic kidney disease, NAFLD, and dyslipidemia, ranging from the molecular and cellular pathogenetic pathways to novel pharmacological and molecular targets for relevant treatments. Original research articles and reviews on these and related topics are welcomed in this Special Issue.

Prof. Dr. Eva Kassi
Dr. Ioannis Kyrou
Prof. Dr. Harpal S. Randeva
Guest Editors

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Keywords

cardiovascular endocrinology
atherosclerosis
coronary artery disease
endocrine hypertension
non-alcoholic fatty liver disease (NAFLD)
diabetes mellitus and obesity
metabolic syndrome
endothelial cells
vascular inflammation
antidiabetic drugs
antihypertensive treatments
lipid lowering treatments
lifestyle interventions
molecular targeted therapies
heart failure
chronic kidney disease

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Published Papers (7 papers)

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Research

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20 pages, 2758 KiB

Open AccessArticle

Knock-Out of IKKepsilon Ameliorates Atherosclerosis and Fatty Liver Disease by Alterations of Lipid Metabolism in the PCSK9 Model in Mice

by Ulrike Weiss, Eleonora Mungo, Michelle Haß, Denis Benning, Robert Gurke, Lisa Hahnefeld, Erika Dorochow, Jessica Schlaudraff, Tobias Schmid, Silvia Kuntschar, Sofie Meyer, Rebekka Medert, Marc Freichel, Gerd Geisslinger and Ellen Niederberger

Int. J. Mol. Sci. 2024, 25(19), 10721; https://doi.org/10.3390/ijms251910721 - 5 Oct 2024

Viewed by 1680

Abstract

The inhibitor-kappaB kinase epsilon (IKKε) represents a non-canonical IκB kinase that modulates NF-κB activity and interferon I responses. Inhibition of this pathway has been linked with atherosclerosis and metabolic dysfunction-associated steatotic liver disease (MASLD), yet the results are contradictory. In this study, we employed a combined model of hepatic PCSK9^D377Y overexpression and a high-fat diet for 16 weeks to induce atherosclerosis and liver steatosis. The development of atherosclerotic plaques, serum lipid concentrations, and lipid metabolism in the liver and adipose tissue were compared between wild-type and IKKε knock-out mice. The formation and progression of plaques were markedly reduced in IKKε knockout mice, accompanied by reduced serum cholesterol levels, fat deposition, and macrophage infiltration within the plaque. Additionally, the development of a fatty liver was diminished in these mice, which may be attributed to decreased levels of multiple lipid species, particularly monounsaturated fatty acids, triglycerides, and ceramides in the serum. The modulation of several proteins within the liver and adipose tissue suggests that de novo lipogenesis and the inflammatory response are suppressed as a consequence of IKKε inhibition. In conclusion, our data suggest that the knockout of IKKε is involved in mechanisms of both atherosclerosis and MASLD. Inhibition of this pathway may therefore represent a novel approach to the treatment of cardiovascular and metabolic diseases. Full article

(This article belongs to the Special Issue Molecular and Translational Research in Cardiovascular Endocrinology, Cardio-Metabolic Diseases and Non-Alcoholic Fatty Liver Disease (NAFLD): 2nd Edition)

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17 pages, 1118 KiB

Open AccessArticle

Okinawa-Based Nordic Diet Decreases Plasma Levels of IAPP and IgA against IAPP Oligomers in Type 2 Diabetes Patients

by Dovilė Pocevičiūtė, Bodil Roth, Bodil Ohlsson and Malin Wennström

Int. J. Mol. Sci. 2024, 25(14), 7665; https://doi.org/10.3390/ijms25147665 - 12 Jul 2024

Cited by 1 | Viewed by 1197

Abstract

Pancreas-derived islet amyloid polypeptide (IAPP) aggregates and deposits in the pancreas and periphery of Type 2 Diabetes (T2D) patients, contributing to diabetic complications. The excess IAPP can be removed by autoantibodies, and increased levels of immunoglobulin (Ig) G against IAPP have been reported in T2D patients. However, whether other Ig classes are also affected and if the levels can be managed is less known. This pre–post study examines IgA levels against IAPP oligomers (IAPP_O-IgA) in T2D patients and assesses the impact of the Okinawa-based Nordic (O-BN) diet—a low-carbohydrate, high-fiber diet—on these levels after following the diet for 3 months. IAPP, IAPP_O-IgA, and total IgA levels were measured in plasma and fecal samples from n = 30 T2D patients collected at baseline, after 3 months of diet, and after additional 4 months of unrestricted diets (a clinical follow-up). The IAPP and IAPP_O-IgA levels were significantly lower after 3 months, with the latter also being significantly reduced at the clinical follow-up. The reduction in plasma IAPP and IAPP_O-IgA levels correlated with reductions in plasma levels of metabolic and inflammatory markers. Hence, following the O-BN diet for at least 3 months is sufficient to reduce circulating IAPP and IAPP_O-IgA levels, which may be principal in managing T2D. Full article

(This article belongs to the Special Issue Molecular and Translational Research in Cardiovascular Endocrinology, Cardio-Metabolic Diseases and Non-Alcoholic Fatty Liver Disease (NAFLD): 2nd Edition)

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16 pages, 1660 KiB

Open AccessArticle

Lipid Emulsions Inhibit Labetalol-Induced Vasodilation in the Isolated Rat Aorta

by Soohee Lee, Kyeong-Eon Park, Yeran Hwang, Sungil Bae, Seong-Ho Ok, Seung-Hyun Ahn, Gyujin Sim, Hyun-Jin Kim, Seunghyeon Park and Ju-Tae Sohn

Int. J. Mol. Sci. 2024, 25(13), 7243; https://doi.org/10.3390/ijms25137243 - 30 Jun 2024

Cited by 2 | Viewed by 1147

Abstract

Lipid emulsions are used as adjuvant drugs to alleviate intractable cardiovascular collapse induced by drug toxicity. We aimed to examine the effect of lipid emulsions on labetalol-induced vasodilation and the underlying mechanism in the isolated rat aorta. We studied the effects of endothelial denudation, N^W-nitro-l-arginine methyl ester (l-NAME), calmidazolium, methylene blue, 1H-[1,2,4]oxadiazolo[4,3-a] quinoxalin-1-one (ODQ), and lipid emulsions on labetalol-induced vasodilation. We also evaluated the effects of lipid emulsions on cyclic guanosine monophosphate (cGMP) formation, endothelial nitric oxide synthase (eNOS) phosphorylation, and endothelial calcium levels induced by labetalol. Labetalol-induced vasodilation was higher in endothelium-intact aortas than that in endothelium-denuded aortas. l-NAME, calmidazolium, methylene blue, and ODQ inhibited labetalol-induced vasodilation in endothelium-intact aortas. Lipid emulsions inhibited labetalol-induced vasodilation in endothelium-intact and endothelium-denuded aortas. l-NAME, ODQ, and lipid emulsions inhibited labetalol-induced cGMP formation in endothelium-intact aortas. Lipid emulsions reversed the stimulatory and inhibitory eNOS (Ser1177 and Thr495) phosphorylation induced by labetalol in human umbilical vein endothelial cells and inhibited the labetalol-induced endothelial calcium increase. Moreover, it decreased labetalol concentration. These results suggest that lipid emulsions inhibit vasodilation induced by toxic doses of labetalol, which is mediated by the inhibition of endothelial nitric oxide release and reduction of labetalol concentration. Full article

(This article belongs to the Special Issue Molecular and Translational Research in Cardiovascular Endocrinology, Cardio-Metabolic Diseases and Non-Alcoholic Fatty Liver Disease (NAFLD): 2nd Edition)

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Review

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54 pages, 2875 KiB

Open AccessReview

Targeting Metabolism: Innovative Therapies for MASLD Unveiled

by Weixin Wang, Xin Gao, Wentong Niu, Jinping Yin and Kan He

Int. J. Mol. Sci. 2025, 26(9), 4077; https://doi.org/10.3390/ijms26094077 - 25 Apr 2025

Viewed by 262

Abstract

The recent introduction of the term metabolic-dysfunction-associated steatotic liver disease (MASLD) has highlighted the critical role of metabolism in the disease’s pathophysiology. This innovative nomenclature signifies a shift from the previous designation of non-alcoholic fatty liver disease (NAFLD), emphasizing the condition’s progressive nature. Simultaneously, MASLD has become one of the most prevalent liver diseases worldwide, highlighting the urgent need for research to elucidate its etiology and develop effective treatment strategies. This review examines and delineates the revised definition of MASLD, exploring its epidemiology and the pathological changes occurring at various stages of the disease. Additionally, it identifies metabolically relevant targets within MASLD and provides a summary of the latest metabolically targeted drugs under development, including those in clinical and some preclinical stages. The review finishes with a look ahead to the future of targeted therapy for MASLD, with the goal of summarizing and providing fresh ideas and insights. Full article

(This article belongs to the Special Issue Molecular and Translational Research in Cardiovascular Endocrinology, Cardio-Metabolic Diseases and Non-Alcoholic Fatty Liver Disease (NAFLD): 2nd Edition)

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42 pages, 3589 KiB

Open AccessReview

Unraveling Metabolic Dysfunction-Associated Steatotic Liver Disease Through the Use of Omics Technologies

by Maria V. Bourganou, Maria Eleni Chondrogianni, Ioannis Kyrou, Christina-Maria Flessa, Antonios Chatzigeorgiou, Evangelos Oikonomou, Vaia Lambadiari, Harpal S. Randeva and Eva Kassi

Int. J. Mol. Sci. 2025, 26(4), 1589; https://doi.org/10.3390/ijms26041589 - 13 Feb 2025

Cited by 1 | Viewed by 1933

Abstract

Non-alcoholic fatty liver disease (NAFLD), now referred to as metabolic dysfunction-associated steatotic liver disease (MASLD), is the most prevalent liver disorder globally, linked to obesity, type 2 diabetes, and cardiovascular risk. Understanding its potential progression from simple steatosis to cirrhosis and hepatocellular carcinoma (HCC) is crucial for patient management and treatment strategies. The disease’s complexity requires innovative approaches for early detection and personalized care. Omics technologies—such as genomics, transcriptomics, proteomics, metabolomics, and exposomics—are revolutionizing the study of MASLD. These high-throughput techniques allow for a deeper exploration of the molecular mechanisms driving disease progression. Genomics can identify genetic predispositions, whilst transcriptomics and proteomics reveal changes in gene expression and protein profiles during disease evolution. Metabolomics offers insights into the metabolic alterations associated with MASLD, while exposomics links environmental exposures to MASLD progression and pathology. By integrating data from various omics platforms, researchers can map out the intricate biochemical pathways involved in liver disease progression. This review discusses the roles of omics technologies in enhancing the understanding of disease progression and highlights potential diagnostic and therapeutic targets within the MASLD spectrum, emphasizing the need for non-invasive tools in disease staging and treatment development. Full article

(This article belongs to the Special Issue Molecular and Translational Research in Cardiovascular Endocrinology, Cardio-Metabolic Diseases and Non-Alcoholic Fatty Liver Disease (NAFLD): 2nd Edition)

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16 pages, 1439 KiB

Open AccessReview

Automaticity of the Pulmonary Vein Myocardium and the Effect of Class I Antiarrhythmic Drugs

by Iyuki Namekata, Maika Seki, Taro Saito, Ryosuke Odaka, Shogo Hamaguchi and Hikaru Tanaka

Int. J. Mol. Sci. 2024, 25(22), 12367; https://doi.org/10.3390/ijms252212367 - 18 Nov 2024

Viewed by 841

Abstract

The pulmonary vein wall contains a myocardial layer whose ectopic automaticity is the major cause of atrial fibrillation. This review summarizes the results obtained in isolated pulmonary vein myocardium from small experimental animals, focusing on the studies with the guinea pig. The diversity in the action potential waveform reflects the difference in the repolarizing potassium channel currents involved. The diastolic depolarization, the trigger of automatic action potentials, is caused by multiple membrane currents, including the Na⁺-Ca²⁺ exchanger current and late I_Na. The action potential waveform and automaticity are affected differentially by α- and β-adrenoceptor stimulation. Class I antiarrhythmic drugs block the propagation of ectopic electrical activity of the pulmonary vein myocardium through blockade of the peak I_Na. Some of the class I antiarrhythmic drugs block the late I_Na and inhibit pulmonary vein automaticity. The negative inotropic and chronotropic effects of class I antiarrhythmic drugs could be largely attributed to their blocking effect on the Ca²⁺ channel rather than the Na⁺ channel. Such a comprehensive understanding of pulmonary vein automaticity and class I antiarrhythmic drugs would lead to an improvement in pharmacotherapy and the development of novel therapeutic agents for atrial fibrillation. Full article

(This article belongs to the Special Issue Molecular and Translational Research in Cardiovascular Endocrinology, Cardio-Metabolic Diseases and Non-Alcoholic Fatty Liver Disease (NAFLD): 2nd Edition)

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24 pages, 1229 KiB

Open AccessReview

Lipoprotein Lipidomics as a Frontier in Non-Alcoholic Fatty Liver Disease Biomarker Discovery

by Luis V. Herrera-Marcos, Jose M. Arbones-Mainar and Jesús Osada

Int. J. Mol. Sci. 2024, 25(15), 8285; https://doi.org/10.3390/ijms25158285 - 29 Jul 2024

Cited by 2 | Viewed by 2039

Abstract

Non-alcoholic fatty liver disease (NAFLD) is a progressive liver disease characterized by the build-up of fat in the liver of individuals in the absence of alcohol consumption. This condition has become a burden in modern societies aggravated by the lack of appropriate predictive biomarkers (other than liver biopsy). To better understand this disease and to find appropriate biomarkers, a new technology has emerged in the last two decades with the ability to explore the unmapped role of lipids in this disease: lipidomics. This technology, based on the combination of chromatography and mass spectrometry, has been extensively used to explore the lipid metabolism of NAFLD. In this review, we aim to summarize the knowledge gained through lipidomics assays exploring tissues, plasma, and lipoproteins from individuals with NAFLD. Our goal is to identify common features and active pathways that could facilitate the finding of a reliable biomarker from this field. The most frequent observation was a variable decrease (1–9%) in polyunsaturated fatty acids in phospholipids and non-esterified fatty acids in NAFLD patients, both in plasma and liver. Additionally, a reduction in phosphatidylcholines is a common feature in the liver. Due to the scarcity of studies, further research is needed to properly detect lipoprotein, plasma, and tissue lipid signatures of NAFLD etiologies, and NAFLD subtypes, and to define the relevance of this technology in disease management strategies in the push toward personalized medicine. Full article

(This article belongs to the Special Issue Molecular and Translational Research in Cardiovascular Endocrinology, Cardio-Metabolic Diseases and Non-Alcoholic Fatty Liver Disease (NAFLD): 2nd Edition)

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