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Biomedicines
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Feature Reviews on Cardiovascular and Metabolic Diseases
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Feature Reviews on Cardiovascular and Metabolic Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 31 March 2025 | Viewed by 1272

Special Issue Editor

Dr. Cristiana Bustea

E-Mail Website
Guest Editor
Department of Preclinical Disciplines, Faculty of Medicine and Pharmacy, University of Oradea, 410073 Oradea, Romania
Interests: hypertension; clinical cardiology; heart failure; echocardiography; myocardial infarction; atherosclerosis; blood pressure; atrial fibrillation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

For a long time, cardiovascular and metabolic diseases have been two of the most significant global health challenges, contributing to a substantial burden of morbidity and mortality worldwide. As our understanding of these complex and interrelated conditions advances, it is essential to synthesize the latest developments and emerging trends to foster better prevention, diagnosis, and treatment strategies. This Special Issue aims to provide a comprehensive overview of the current state of knowledge in these fields. By focusing on the intersections between cardiovascular and metabolic health, or either of them separately, this collection of reviews will offer valuable insights into the underlying mechanisms driving disease progression, as well as innovative approaches to managing these conditions in the face of their rising global prevalence. We hope that this Special Issue will serve as a useful resource for researchers, clinicians, and scholars committed to advancing health in these areas.

This Special Issue welcomes all up-to-date review articles that address recent research and developments in cardiovascular and metabolic diseases.

Dr. Cristiana Bustea
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. Biomedicines 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 2600 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

  • cardiovascular diseases
  • metabolic diseases
  • global health
  • disease prevention
  • innovative treatments

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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Review

13 pages, 1552 KiB  
Review
The Genetic Mechanisms and Pathology of Atrial Fibrillation: A Narrative Review
by Elio Zito, Lorenzo Bianchini, Elena Sommariva, Mariabeatrice Costa, Giovanni B. Forleo, Claudio Tondo and Marco Schiavone
Biomedicines 2025, 13(3), 654; https://doi.org/10.3390/biomedicines13030654 - 7 Mar 2025
Viewed by 195
Abstract
Atrial fibrillation (AF), the most prevalent tachyarrhythmia worldwide, is a complex condition influenced by genetic, structural, and environmental factors. While AF in the elderly is often associated with underlying cardiac disease, early-onset or “lone” AF (LAF) exhibits a stronger genetic predisposition. Studies have [...] Read more.
Atrial fibrillation (AF), the most prevalent tachyarrhythmia worldwide, is a complex condition influenced by genetic, structural, and environmental factors. While AF in the elderly is often associated with underlying cardiac disease, early-onset or “lone” AF (LAF) exhibits a stronger genetic predisposition. Studies have identified both monogenic and polygenic contributors to AF risk. Monogenic mutations, inherited in Mendelian patterns, often affect ion channels and regulatory proteins, while polygenic variants modulate susceptibility and interact with environmental factors. Genome-wide association studies (GWAS) and exosome-wide association studies (ExWAS) have expanded our understanding of AF genetics, identifying numerous susceptibility loci, though challenges remain in linking these variants to specific molecular mechanisms. Pathophysiologically, AF results from a balance of triggers, drivers, and substrates. Triggers, such as ectopic foci in the pulmonary veins, initiate AF episodes, while structural and electrical remodeling perpetuates the arrhythmia. Fibrosis, atrial dilation, and tachycardia-induced remodeling promote reentry circuits and irregular conduction, increasing AF vulnerability. The interplay between genetic predisposition and remodeling processes underscores the complexity of AF maintenance, particularly in persistent AF forms. Emerging insights into AF genetics and pathophysiology highlight the need for personalized approaches to its prevention and management. Understanding genetic risk, combined with targeted therapies addressing structural and electrical remodeling, holds promise for improved patient outcomes. Future research into AF’s molecular and genetic mechanisms will be key to advancing precision medicine in this field. Full article
(This article belongs to the Special Issue Feature Reviews on Cardiovascular and Metabolic Diseases)
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Figure 1

Figure 1
<p>A PRS is calculated for each individual as a sum of the product of genetic dosage and a weight. The weights are derived from the effect estimates of a GWAS. The PRS of individuals in a population follows a gaussian distribution. Individuals in the highest percentile of the distribution show an increased risk for AF versus the remaining population. PRS: polygenic risk score; adapted from Roselli et al. [<a href="#B38-biomedicines-13-00654" class="html-bibr">38</a>].</p> Full article ">Figure 2
<p>Schematic representation of AF progression process from paroxysmal to persistent.</p> Full article ">Figure 3
<p>AF-mediated ion channel alterations. ATR is associated with (1) peak INa reduction due to Na<sup>+</sup> channel downregulation, which leads to lower energy source and therefore lower conduction velocity; (2) lower ICaL during AP phase 2, which reduces APD, and (3) higher IK1 and IKAch and therefore lower APD and RP. ATR: atrial tachyarrhythmia remodeling; APD: action potential duration; CV: conduction velocity; RP: refractory period; INa: Na<sup>+</sup> channel current; ICaL: L-type Ca<sup>2+</sup> channel current; IK1: K<sup>+</sup> inward rectifier channel current; IKAch: acetylcholine-regulated K<sup>+</sup> channel current.</p> Full article ">
21 pages, 3188 KiB  
Review
Effects of Weight Loss on Endothelium and Vascular Homeostasis: Impact on Cardiovascular Risk
by Margherita Tiezzi, Francesco Vieceli Dalla Sega, Paolo Gentileschi, Michela Campanelli, Domenico Benavoli and Elena Tremoli
Biomedicines 2025, 13(2), 381; https://doi.org/10.3390/biomedicines13020381 - 6 Feb 2025
Viewed by 569
Abstract
Available knowledge shows that obesity is associated with an impaired endothelial function and an increase in cardiovascular risk, but the mechanisms of this association are not yet fully understood. Adipose tissue dysfunction, adipocytokines production, along with systemic inflammation and associated comorbidities (e.g., diabetes [...] Read more.
Available knowledge shows that obesity is associated with an impaired endothelial function and an increase in cardiovascular risk, but the mechanisms of this association are not yet fully understood. Adipose tissue dysfunction, adipocytokines production, along with systemic inflammation and associated comorbidities (e.g., diabetes and hypertension), are regarded as the primary physiological and pathological factors. Various strategies are now available for the control of excess body weight. Dietary regimens alone, or in association with bariatric surgery when indicated, are now widely used. Of particular interest is the understanding of the effect of these interventions on endothelial homeostasis in relation to cardiovascular health. Substantial weight loss resulting from both diet and bariatric surgery decreases circulating biomarkers and improves endothelial function. Extensive clinical trials and meta-analyses show that bariatric surgery (particularly gastric bypass) has more substantial and long-lasting effect on weight loss and glucose regulation, as well as on distinct circulating biomarkers of cardiovascular risk. This review summarizes the current understanding of the distinct effects of diet-induced and surgery-induced weight loss on endothelial function, focusing on the key mechanisms involved in these effects. Full article
(This article belongs to the Special Issue Feature Reviews on Cardiovascular and Metabolic Diseases)
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Figure 1

Figure 1
<p>Different types of adipose tissue. White adipose tissue (WAT) is the most represented type of AT, while brown represents around 4% of total fat and beige 1–2%. White and brown AT originate from cells being different both from the structural and functional standpoints. It has a lower concentration of mitochondria compared to other AT types. WAT directly mediates endothelial dysfunction via the secretion of cytokines and mediators involved in vascular pathophysiology. Brown adipose tissue (BAT) bears a thermogenic action and thus it displays higher numbers of mitochondria. It increases triglyceride clearance and insulin sensitivity and produces mediators involved in the angiogenesis and the lowering of the vascular inflammation, globally playing a cardio- and a vasculo-protective function. Beige adipose tissue is an intermediate entity which appears less detrimental to CV health, with research still ongoing. Upon stimulation, WAT can transform into beige (“WAT browning”), with a mechanism that is reversible upon the stimulus’ withdrawal. The continuous arrows between WAT-beige AT and between BAT-WAT indicate the possibility of AT transformation depending on the presence of different stimuli.. Similarly, BAT can undergo a “whitening” process, especially in the presence of metabolic alterations. ↓: decrease; ↑: increase; AT: adipose tissue, ECs: endothelial cells, FGF21: fibroblast growth factor 21, FFAs: free fatty acids. Image created with Biorender (<a href="http://www.biorender.com" target="_blank">www.biorender.com</a>, accessed on 27 January 2025).</p> Full article ">Figure 2
<p>Schematic representation of potential vascular effects of diet-induced weight loss (DIWL). Diet-induced weight loss induces metabolic changes and positively influence endothelial health. After DIWL, a decrease in circulating biomarkers of vascular and endothelial damage is described, together with an improvement in endothelial function and remodelling (increased FMD, decreased pulse wave velocity, increased retinal arteriolar calibre). ↓: decrease; ↑: increase. ICAM-1: intercellular adhesion molecule 1, VCAM-1: vascular cell adhesion molecule 1, PAI-1: plasminogen activator inhibitor 1, VEGF: vascular endothelial growth factor, IL6. Interleukin 6, TNF: tumor necrosis factor, FMD: flow-mediated dilation, PWV: pulse wave velocity. Image created with Biorender (<a href="http://www.biorender.com" target="_blank">www.biorender.com</a>, accessed on 27 January 2025).</p> Full article ">Figure 3
<p>Schematic representation of vascular effects of surgery-induced weight loss (SIWL). After bariatric surgery, an improvement in circulating biomarkers involved in vascular homeostasis is observed. Moreover, patients display improved endothelial function (increased FMD, and endothelium-dependent vasodilation) and vascular remodelling, represented by a decrease in intima-media thickness and an increase in brachial arterial diameter. Notably, hybrid surgical techniques exist combining both restrictive and malabsorptive BS. ↓: decrease; ↑: increase. CV: cardiovascular, ICAM1: intercellular adhesion molecule 1, VEGF-A: vascular endothelial growth factor A, PAI-1: plasminogen activator inhibitor-1, FMD: flow-mediated dilation, IMT: intima-media thickness, RYGB: Roux-en-Y gastric bypass, BPD: biliopancreatic diversion. Image created with Biorender (<a href="http://www.biorender.com" target="_blank">www.biorender.com</a>, accessed on 27 January 2025).</p> Full article ">Figure 4
<p>The main actions that GLP-1 exerts on the cardiovascular system, based on the available scientific evidence from human and animal models. GLP-1 secretion is stimulated by food transit in the gastrointestinal tract. GLP-1 exerts metabolic and vasculo-protective actions, both contributing to an improvement in the CV outcome. For instance, GLP-1 can increase myocardial glucose uptake and decrease oxidative stress and cardiomyocytes apoptosis, while improving NO release and natriuresis, positively affecting vascular tone. ↓: decrease; ↑: increase. Positive signs in green indicate stimulation. Green arrows indicate production. GLP-1: glucagon-like peptide 1; GLP-1R: GLP-1 receptor; CNS: central nervous system; NO: nitric oxide; RAS: renin angiotensin system; Ang II: angiotensin II. Image created with Biorender (<a href="http://www.biorender.com" target="_blank">www.biorender.com</a>, accessed on 27 January 2025).</p> Full article ">Figure 5
<p>The Main actions of ghrelin on the cardiovascular system, based on available scientific evidence from human and animal models. In the conditions of a negative energy balance, ghrelin is produced by the gastric fundus and induces the synthesis of anabolic mediators at the central nervous system level. In parallel, it can impact the CV system. Preliminary data indicate that unacylated ghrelin (UAG) ameliorates vascular endothelial function, as compared to the acylated form (AG), but further research is needed. A crosstalk between ghrelin action and glucose metabolism is observed, as insulin contributes to increased NO bioavailability via the activation of PI3K/Akt pathway, as does ghrelin. ↓: decrease; ↑: increase. Positive signs in green indicate stimulation. Green arrows indicate production. GHS-R: growth hormone segretagogue receptor, GOAT: ghrelin O-acyltransferase, AgRP: agouti-related protein, NPY: neuropeptide Y, ACTH: adrenocorticotropic hormone, GH: growth hormone, IGF-1: insulin-like growth factor 1, NO: nitric oxide, PI3K: phosphoinositide 3-kinase, Akt: Akt serine-threonine protein kinase. Image created with Biorender (<a href="http://www.biorender.com" target="_blank">www.biorender.com</a>, accessed on 27 January 2025).</p> Full article ">Figure 6
<p>The main actions adiponectin exerts on the cardiovascular system, based on the available scientific evidence from human and animal models. In healthy conditions, adiponectin is produced by the adipocytes in three isoforms with different molecular weights. The beneficial roles of adiponectin on the cardiovascular system are mediated by three peripheral receptors (AdipoR1 to 3) that are expressed in different cell types, including endothelial cells and vascular smooth muscle cells. Adiponectin can improve endothelial function by directing increasing NO bioavailability and reducing LDL uptake and accumulation within the vascular wall. It can also ameliorate glucose metabolism (indirectly promoting vascular homeostasis) and attenuates negative vascular remodelling via decreased vascular smooth muscle cells migration and proliferation. Ultimately, it blocks NF-kB signalling, reducing vascular inflammation and apoptosis. ↓: decrease; ↑: increase. Green arrow indicates production. ICAM-1: intercellular adhesion molecule 1, VCAM-1: vascular cell adhesion molecule 1, NO: nitric oxide, LDL: low-density lipoprotein, VSMCs: vascular smooth muscle cells, NF-kB: nuclear factor kB, ECs: endothelial cells. Image created with Biorender (<a href="http://www.biorender.com" target="_blank">www.biorender.com</a>, accessed on 27 January 2025).</p> Full article ">Figure 7
<p>The main actions leptin exerts on the cardiovascular system, based on the available scientific evidence from human and animal models. Leptin is mainly produced by adipose tissue in response to increased food intake and insulin levels. Its action is essentially anorexigenic (stimulates satiety), but different effects on the CV system were described—predominantly in animal models—suggesting that only normal leptin values provide CV protection, whereas any other variation from a set point might negatively affect the CV system. Besides, leptin can stimulate sympathetic activity, an action that is maintained even in leptin-resistance conditions. ↓: decrease; ↑: increase. Positive signs in green indicate stimulation. Green arrows indicate production. Blue line indicates inhibition. WAT: white adipose tissue, AgRP: agouti-related protein, NPY: neuropeptide Y, POMC: proopiomelanocortin, LVH: left ventricular hypertrophy, CV: cardiovascular. Image created with Biorender (<a href="http://www.biorender.com" target="_blank">www.biorender.com</a>, accessed on 27 January 2025).</p> Full article ">
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