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Molecular and Translational Research in Cardiovascular Endocrinology, Cardio-Metabolic Diseases and Non-alcoholic Fatty Liver Disease (NAFLD)

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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: 31 May 2024 | Viewed by 15057

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Special Issue Editors

Prof. Dr. Eva Kassi

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Guest Editor

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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Guest Editor

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

Prof. Dr. Harpal S. Randeva

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Guest Editor

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
Interests: women's health; endocrinology; gynaecological cancers; PCOS; metabolism; nutrition; diabetes; endocrine-disrupting chemicals (EDCs); links between obesity and cancer
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiovascular tissues have been recognized as dynamic endocrine organs, with vital stimuli that affect the cardiovascular system by 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 the risk of cardiovascular disease (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., antihypertensive lipid-lowering treatments, antidiabetic drugs , etc.), which may target more than one aspect/factor of cardiometabolic diseases.

This Special Issue, which is edited by Prof. Dr. E. Kassi, As. Prof. Dr. I. Kyrou and Prof. Dr. 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, with topics 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 welcome in this Special Issue.

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

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

Published Papers (9 papers)

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Research

Jump to: Review

12 pages, 1693 KiB

Open AccessArticle

Impact of Glucagon-Like Peptide 1 Receptor Agonists on Biochemical Markers of the Initiation of Atherosclerotic Process

by Marcin Hachuła, Michał Kosowski, Sabina Ryl, Marcin Basiak and Bogusław Okopień

Int. J. Mol. Sci. 2024, 25(3), 1854; https://doi.org/10.3390/ijms25031854 - 03 Feb 2024

Viewed by 907

Abstract

Atherosclerosis stands out as one of the leading causes of global mortality. The inflammatory response against vascular wall components plays a pivotal role in the atherogenic process. The initiation of this process is notably driven by oxidized low-density lipoprotein (oxLDL) and a range of pro-inflammatory cytokines, with interleukin-1β (Il-1β) and tumor necrosis factor α (TNFα) emerging as particularly significant in the early stages of atherosclerotic plaque formation. In recent years, researchers worldwide have been diligently exploring innovative therapeutic approaches for metabolic diseases, recognizing their impact on the atherogenesis process. Our study aimed to investigate the influence of glucagon-like peptide 1 receptor agonists (GLP-1RA) on cytokine concentrations associated with the initiation of atherosclerotic plaque formation in a group of patients with type 2 diabetes and dyslipidemia. The study encompassed 50 subjects aged 41–81 (mean: 60.7), all diagnosed with type 2 diabetes, dyslipidemia and confirmed atherosclerosis based on B-mode ultrasound. Following a 180-day treatment with dulaglutide or semaglutide, we observed a statistically significant reduction in biochemical markers (oxLDL, TNFα and Il-1β) associated with the initiation of the atherosclerotic process (p < 0.001) within our study group. In addition to the already acknowledged positive effects of GLP-1RA on the metabolic parameters of treated patients, these drugs demonstrated a notable reduction in proinflammatory cytokine concentrations and may constitute an important element of therapy aimed at reducing cardiovascular risk. 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))

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17 pages, 2664 KiB

Open AccessArticle

Comprehensive Analysis of 1-Year-Old Female Apolipoprotein E-Deficient Mice Reveals Advanced Atherosclerosis with Vulnerable Plaque Characteristics

by Sotirios Kotsovilis, Maria Salagianni, Aimilia Varela, Constantinos H. Davos, Ioanna E. Galani and Evangelos Andreakos

Int. J. Mol. Sci. 2024, 25(2), 1355; https://doi.org/10.3390/ijms25021355 - 22 Jan 2024

Viewed by 874

Abstract

Apolipoprotein E-knockout (Apoe-/-) mice constitute the most widely employed animal model of atherosclerosis. Deletion of Apoe induces profound hypercholesterolemia and promotes the development of atherosclerosis. However, despite its widespread use, the Apoe-/- mouse model remains incompletely characterized, especially at late time points and advanced disease stages. Thus, it is unclear how late atherosclerotic plaques compare to earlier ones in terms of lipid deposition, calcification, macrophage accumulation, smooth muscle cell presence, or plaque necrosis. Additionally, it is unknown how cardiac function and hemodynamic parameters are affected at late disease stages. Here, we used a comprehensive analysis based on histology, fluorescence microscopy, and Doppler ultrasonography to show that in normal chow diet-fed Apoe-/- mice, atherosclerotic lesions at the level of the aortic valve evolve from a more cellular macrophage-rich phenotype at 26 weeks to an acellular, lipid-rich, and more necrotic phenotype at 52 weeks of age, also marked by enhanced lipid deposition and calcification. Coronary artery atherosclerotic lesions are sparse at 26 weeks but ubiquitous and extensive at 52 weeks; yet, left ventricular function was not significantly affected. These findings demonstrate that atherosclerosis in Apoe-/- mice is a highly dynamic process, with atherosclerotic plaques evolving over time. At late disease stages, histopathological characteristics of increased plaque vulnerability predominate in combination with frequent and extensive coronary artery lesions, which nevertheless may not necessarily result in impaired cardiac function. 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))

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19 pages, 1760 KiB

Open AccessArticle

Induced Pluripotent Stem Cell-Derived Cardiomyocytes Therapy for Ischemic Heart Disease in Animal Model: A Meta-Analysis

by Quan Duy Vo, Yukihiro Saito, Kazufumi Nakamura, Toshihiro Iida and Shinsuke Yuasa

Int. J. Mol. Sci. 2024, 25(2), 987; https://doi.org/10.3390/ijms25020987 - 12 Jan 2024

Cited by 2 | Viewed by 1187

Abstract

Ischemic heart disease (IHD) poses a significant challenge in cardiovascular health, with current treatments showing limited success. Induced pluripotent derived–cardiomyocyte (iPSC-CM) therapy within regenerative medicine offers potential for IHD patients, although its clinical impacts remain uncertain. This study utilizes meta-analysis to assess iPSC-CM outcomes in terms of efficacy and safety in IHD animal model studies. A meta-analysis encompassing PUBMED, ScienceDirect, Web of Science, and the Cochrane Library databases, from inception until October 2023, investigated iPSC therapy effects on cardiac function and safety outcomes. Among 51 eligible studies involving 1012 animals, despite substantial heterogeneity, the iPSC-CM transplantation improved left ventricular ejection fraction (LVEF) by 8.23% (95% CI, 7.15 to 9.32%; p < 0.001) compared to control groups. Additionally, cell-based treatment reduced the left ventricle fibrosis area and showed a tendency to reduce left ventricular end-systolic volume (LVESV) and end-diastolic volume (LVEDV). No significant differences emerged in mortality and arrhythmia risk between iPSC-CM treatment and control groups. In conclusion, this meta-analysis indicates iPSC-CM therapy’s promise as a safe and beneficial intervention for enhancing heart function in IHD. However, due to observed heterogeneity, the efficacy of this treatment must be further explored through large randomized controlled trials based on rigorous research design. 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))

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19 pages, 5677 KiB

Open AccessArticle

Impact of Vancomycin Treatment and Gut Microbiota on Bile Acid Metabolism and the Development of Non-Alcoholic Steatohepatitis in Mice

by Kaichi Kasai, Naoya Igarashi, Yuki Tada, Koudai Kani, Shun Takano, Tsutomu Yanagibashi, Fumitake Usui-Kawanishi, Shiho Fujisaka, Shiro Watanabe, Mayuko Ichimura-Shimizu, Kiyoshi Takatsu, Kazuyuki Tobe, Koichi Tsuneyama, Yukihiro Furusawa and Yoshinori Nagai

Int. J. Mol. Sci. 2023, 24(4), 4050; https://doi.org/10.3390/ijms24044050 - 17 Feb 2023

Cited by 2 | Viewed by 2665

Abstract

The potential roles of the gut microbiota in the pathogenesis of non-alcoholic fatty liver disease, including non-alcoholic steatohepatitis (NASH), have attracted increased interest. We have investigated the links between gut microbiota and NASH development in Tsumura-Suzuki non-obese mice fed a high-fat/cholesterol/cholate-based (iHFC) diet that exhibit advanced liver fibrosis using antibiotic treatments. The administration of vancomycin, which targets Gram-positive organisms, exacerbated the progression of liver damage, steatohepatitis, and fibrosis in iHFC-fed mice, but not in mice fed a normal diet. F4/80⁺-recruited macrophages were more abundant in the liver of vancomycin-treated iHFC-fed mice. The infiltration of CD11c⁺-recruited macrophages into the liver, forming hepatic crown-like structures, was enhanced by vancomycin treatment. The co-localization of this macrophage subset with collagen was greatly augmented in the liver of vancomycin-treated iHFC-fed mice. These changes were rarely seen with the administration of metronidazole, which targets anaerobic organisms, in iHFC-fed mice. Finally, the vancomycin treatment dramatically modulated the level and composition of bile acid in iHFC-fed mice. Thus, our data demonstrate that changes in inflammation and fibrosis in the liver by the iHFC diet can be modified by antibiotic-induced changes in gut microbiota and shed light on their roles in the pathogenesis of advanced liver fibrosis. 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))

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Review

Jump to: Research

19 pages, 1179 KiB

Open AccessReview

Association between Immune Checkpoint Inhibitors and Atherosclerotic Cardiovascular Disease Risk: Another Brick in the Wall

by Linda Piras, Michela Zuccanti, Paola Russo, Francesca Riccio, Antonio Agresti, Camilla Lustri, Domenico Dardani, Armando Ferrera, Vincenzo Fiorentini, Giuliano Tocci, Giacomo Tini Melato, Massimo Volpe, Emanuele Barbato and Allegra Battistoni

Int. J. Mol. Sci. 2024, 25(5), 2502; https://doi.org/10.3390/ijms25052502 - 21 Feb 2024

Viewed by 979

Abstract

In recent years, immune checkpoint inhibitors have significantly changed the field of oncology, emerging as first-line treatment, either alone or in combination with other regimens, for numerous malignancies, improving overall survival and progression-free survival in these patients. However, immune checkpoint inhibitors might also cause severe or fatal immune-related adverse events, including adverse cardiovascular events. Initially, myocarditis was recognized as the main immune checkpoint inhibitor-related cardiac event, but our knowledge of other potential immune-related cardiovascular adverse events continues to broaden. Recently, preclinical and clinical data seem to support an association between immune checkpoint inhibitors and accelerated atherosclerosis as well as atherosclerotic cardiovascular events such as cardiac ischemic disease, stroke, and peripheral artery disease. In this review, by offering a comprehensive overview of the pivotal role of inflammation in atherosclerosis, we focus on the potential molecular pathways underlying the effects of immune checkpoint inhibitors on cardiovascular diseases. Moreover, we provide an overview of therapeutic strategies for cancer patients undergoing immunotherapy to prevent the development of cardiovascular 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))

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17 pages, 2378 KiB

Open AccessReview

New Insights into the Role of KLF10 in Tissue Fibrosis

by Uzma Yaseen, Soonjae Hwang, Sangbin Park, Soo-Bin Kim, Ho-Jae Lee and Ji-Young Cha

Int. J. Mol. Sci. 2024, 25(2), 1276; https://doi.org/10.3390/ijms25021276 - 20 Jan 2024

Viewed by 990

Abstract

Fibrosis, characterized by excessive extracellular matrix accumulation, disrupts normal tissue architecture, causes organ dysfunction, and contributes to numerous chronic diseases. This review focuses on Krüppel-like factor 10 (KLF10), a transcription factor significantly induced by transforming growth factor-β (TGF-β), and its role in fibrosis pathogenesis and progression across various tissues. KLF10, initially identified as TGF-β-inducible early gene-1 (TIEG1), is involved in key biological processes including cell proliferation, differentiation, apoptosis, and immune responses. Our analysis investigated KLF10 gene and protein structures, interaction partners, and context-dependent functions in fibrotic diseases. This review highlights recent findings that underscore KLF10 interaction with pivotal signaling pathways, such as TGF-β, and the modulation of gene expression in fibrotic tissues. We examined the dual role of KLF10 in promoting and inhibiting fibrosis depending on tissue type and fibrotic context. This review also discusses the therapeutic potential of targeting KLF10 in fibrotic diseases, based on its regulatory role in key pathogenic mechanisms. By consolidating current research, this review aims to enhance the understanding of the multifaceted role of KLF10 in fibrosis and stimulate further research into its potential as a therapeutic target in combating fibrotic 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))

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21 pages, 574 KiB

Open AccessReview

Nrf2 Pathway and Oxidative Stress as a Common Target for Treatment of Diabetes and Its Comorbidities

by Michelle Yi, Leslie Cruz Cisneros, Eric J. Cho, Michael Alexander, Francesca A. Kimelman, Lourdes Swentek, Antoney Ferrey, Ekamol Tantisattamo and Hirohito Ichii

Int. J. Mol. Sci. 2024, 25(2), 821; https://doi.org/10.3390/ijms25020821 - 09 Jan 2024

Viewed by 1438

Abstract

Diabetes is a chronic disease that induces many comorbidities, including cardiovascular disease, nephropathy, and liver damage. Many mechanisms have been suggested as to how diabetes leads to these comorbidities, of which increased oxidative stress in diabetic patients has been strongly implicated. Limited knowledge of antioxidative antidiabetic drugs and substances that can address diabetic comorbidities through the nuclear factor erythroid 2–related factor 2 (Nrf2) pathway calls for detailed investigation. This review will describe how diabetes increases oxidative stress, the general impact of that oxidative stress, and how oxidative stress primarily contributes to diabetic comorbidities. It will also address how treatments for diabetes, especially focusing on their effects on the Nrf2 antioxidative pathway, have been shown to similarly affect the Nrf2 pathway of the heart, kidney, and liver systems. This review demonstrates that the Nrf2 pathway is a common pathogenic component of diabetes and its associated comorbidities, potentially identifying this pathway as a target to guide future treatments. 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))

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11 pages, 1003 KiB

Open AccessReview

Understanding the Relationship between Nonalcoholic Fatty Liver Disease and Thyroid Disease

by Paulina Vidal-Cevallos, Sofía Murúa-Beltrán Gall, Misael Uribe and Norberto C. Chávez-Tapia

Int. J. Mol. Sci. 2023, 24(19), 14605; https://doi.org/10.3390/ijms241914605 - 27 Sep 2023

Cited by 4 | Viewed by 2584

Abstract

The prevalence of hypothyroidism in patients with nonalcoholic fatty liver disease (NAFLD) is high (22.4%). Thyroid hormones (THs) regulate many metabolic activities in the liver by promoting the export and oxidation of lipids, as well as de novo lipogenesis. They also control hepatic insulin sensitivity and suppress hepatic gluconeogenesis. Because of its importance in lipid and carbohydrate metabolism, the involvement of thyroid dysfunction in the pathogenesis of NAFLD seems plausible. The mechanisms implicated in this relationship include high thyroid-stimulating hormone (TSH) levels, low TH levels, and chronic inflammation. The activity of the TH receptor (THR)-β in response to THs is essential in the pathogenesis of hypothyroidism-induced NAFLD. Therefore, an orally active selective liver THR-β agonist, Resmetirom (MGL-3196), was developed, and has been shown to reduce liver fat content, and as a secondary end point, to improve nonalcoholic steatohepatitis. The treatment of NAFLD with THR-β agonists seems quite promising, and other agonists are currently under development and investigation. This review aims to shine a light on the pathophysiological and epidemiological evidence regarding this relationship and the effect that treatment with THs and selective liver THR-β agonists have on hepatic lipid metabolism. 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))

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Graphical abstract

21 pages, 1762 KiB

Open AccessReview

Non-Alcoholic Fatty Liver Disease and Echocardiographic Parameters of Left Ventricular Diastolic Function: A Systematic Review and Meta-Analysis

by Athina Goliopoulou, Panagiotis Theofilis, Evangelos Oikonomou, Artemis Anastasiou, Panteleimon Pantelidis, Maria Ioanna Gounaridi, Georgios E. Zakynthinos, Ourania Katsarou, Eva Kassi, Vaia Lambadiari, Dimitris Tousoulis, Manolis Vavuranakis and Gerasimos Siasos

Int. J. Mol. Sci. 2023, 24(18), 14292; https://doi.org/10.3390/ijms241814292 - 19 Sep 2023

Cited by 1 | Viewed by 1325

Abstract

The cardiovascular implications of non-alcoholic fatty liver disease (NAFLD) have been associated with heart failure with preserved ejection fraction (HFpEF). The purpose of this review was to conduct a bibliographic search regarding the correlation between NAFLD and the echocardiographic parameters of left ventricular diastolic function. A systematic literature search was conducted in PubMed and Embase for original research data reporting on the association of NAFLD with diastolic function markers [E/e′, left atrial volume index (LAVi), left ventricular mass index (LVMi)]. Meta-analysis was performed using the meta and dmetar packages in R studio v.1.4.1106, with p < 0.05 values being considered significant. Results are expressed as the standardized mean difference (SMD) for continuous variables and as the odds ratio (OR) for categorical variables, with respective 95% confidence intervals (CI). Heterogeneity between studies was expressed with index Ι². From the preliminary search, 2619 articles were found from which 31 studies were included in the final statistical analysis. The meta-analysis of 8 studies which reported on the prevalence of diastolic dysfunction showed that it was increased in patients with NAFLD (OR: 2.07, 95% CI 1.24–3.44 with p = 0.01, I²: 80% with p < 0.01). The meta-analysis of 21 studies showed significantly higher E/e′ in NAFLD patients (SMD 1.02, 95% CI 0.43–1.61 with p < 0.001, I²: 97% with p < 0.001). Individuals with NAFLD had increased LAVi (SMD: 0.87, 95% CI 0.38–1.37 with p < 0.001, I²: 96% with p < 0.001) and LVMi (SMD: 0.89, 95% CI 0.31–1.48 with p = 0.003, I²: 100% with p < 0.001). To conclude, in the meta-analysis of 31 observational studies, NAFLD patients were found to have affected left ventricular diastolic function, supporting the hypothesis of NAFLD being associated with HFpEF. 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))

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