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A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (31 August 2024) | Viewed by 28365

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Dr. Delia Lidia Şălaru

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Department of Internal Medicine, Faculty of Medicine, Grigore T. Popa University of Medicine and Pharmacy of Iasi, 16 University Street, 700115 Iasi, Romania
Interests: venous and arterial thrombosisme
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Dear Colleagues,

Cardiovascular diseases result from a complex dysfunction of different effectors, pathways, and molecular circuits. Deciphering the underlying mechanisms of heart and blood vessel diseases, integrating known biology with newly discovered advanced molecular technology, opens a new

perspective on the possibility of the prevention and/or diagnosis of cardiovascular pathology.

In this Special Issue, we invite researchers to submit their findings on novel biomarkers, new pathomechanisms, and emerging therapeutic targets from a molecular point of view regarding the entire spectrum of cardiovascular diseases, from atherosclerosis and atherothrombosis to emerging concepts in heart failure. Molecular substrates in arrhythmias, genetic disorders, and genetic susceptibility, as well as highlights of interactions between other organs and systems and structural cardiac diseases, are more than welcome.

Dr. Delia Lidia Şălaru
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. Current Issues in Molecular Biology 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 2200 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
heart diseases
blood vessel diseases
atherosclerosis
atherothrombosis
heart failure

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Published Papers (9 papers)

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Research

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10 pages, 2740 KiB

Open AccessArticle

Correlation of Eight (8) Polymorphisms and Their Genotypes with the Risk Factors of Cardiovascular Disease in a Black Elderly Population

by Joseph Musonda Chalwe, Christa Johanna Grobler and Wilna Hendrika Oldewage-Theron

Curr. Issues Mol. Biol. 2024, 46(11), 12694-12703; https://doi.org/10.3390/cimb46110753 - 8 Nov 2024

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Abstract

Single nucleotide polymorphisms (SNPs) have been associated with the development of cardiovascular diseases (CVDs). This study correlated eight SNPs with the risk factors of CVD in a black elderly population. Genotyping was used to detect eight polymorphisms; rs675 (ApoA-IV), rs699 (Angiotensinogen (AGT)), rs247616 and rs1968905 (Cholesteryl ester transfer protein (CETP)), rs1801278 (Insulin receptor substrate 1 (IRS-1)), rs1805087 (Methylenetetrahydrofolate reductase (MTHFR)) and rs28362286 and rs67608943 (Proprotein convertase subtilisin/kexin type 9 (PCSK9)), as well as their genotypes in deoxyribonucleic acid (DNA) extracted from peripheral blood. The cardiovascular risk (CVR) measurements were conducted on a Konelab 20i Thermo Scientific autoanalyzer and an enzyme-linked immunoassay (ELISA) assay. International Business Machines Corporation (IBM)^® Statistical Package for the Social Sciences ^® (SPSS) version 28 was used for statistical analysis. The heterozygous and homozygous genotypes of the eight polymorphisms were detected with the corresponding CVD risk factors. Subgroup analysis indicated that certain genotype carriers exhibited variations in their concentrations of CVR factors compared to others; however, these differences did not reach statistical significance. For example, carriers of the G genotype of the rs699 polymorphism showed marginally different blood pressure readings compared to the AG genotype carriers. The multiple linear regression analysis indicated that the only significant association was between PCSK9 and the rs28362286 (p = 0.029) polymorphism. The findings of our study show that single nucleotide polymorphisms are disseminated across the human genome. The heterozygous and homozygous genotypes of the SNPs require further investigation as they may have independent and possible collective roles in increasing the risk of CVDs. Full article

(This article belongs to the Special Issue A Focus on the Molecular Basis of Cardiovascular Diseases)

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17 pages, 3569 KiB

Open AccessArticle

Low Levels of IgM Recognizing 4-Hydroxy-2-Nonenal-Modified Apolipoprotein A-I Peptide and Its Association with the Severity of Coronary Artery Disease in Taiwanese Patients

by Meng-Huan Lei, Po-Wen Hsu, Yin-Tai Tsai, Chen-Chi Chang, I-Jung Tsai, Hung Hsu, Ming-Hui Cheng, Ying-Li Huang, Hung-Tse Lin, Yu-Cheng Hsu and Ching-Yu Lin

Curr. Issues Mol. Biol. 2024, 46(6), 6267-6283; https://doi.org/10.3390/cimb46060374 - 20 Jun 2024

Cited by 1 | Viewed by 1172

Abstract

Autoantibodies against apolipoprotein A-I (ApoA-I) are associated with cardiovascular disease risks. We aimed to examine the 4-hydroxy-2-nonenal (HNE) modification of ApoA-I in coronary artery disease (CAD) and evaluate the potential risk of autoantibodies against their unmodified and HNE-modified peptides. We assessed plasma levels of ApoA-I, HNE-protein adducts, and autoantibodies against unmodified and HNE-peptide adducts, and significant correlations and odds ratios (ORs) were examined. Two novel CAD-specific HNE-peptide adducts, ApoA-I^251–262 and ApoA-I^70–83, were identified. Notably, immunoglobulin G (IgG) anti-ApoA-I^251–262 HNE, IgM anti-ApoA-I^70–83 HNE, IgG anti-ApoA-I^251–262, IgG anti-ApoA-I^70–83, and HNE-protein adducts were significantly correlated with triglycerides, creatinine, or high-density lipoprotein in CAD with various degrees of stenosis (<30% or >70%). The HNE-protein adduct (OR = 2.208-fold, p = 0.020) and IgM anti-ApoA-I^251–262 HNE (2.046-fold, p = 0.035) showed an increased risk of progression from >30% stenosis in CAD. HNE-protein adducts and IgM anti-ApoA-I^251–262 HNE may increase the severity of CAD at high and low levels, respectively. Full article

(This article belongs to the Special Issue A Focus on the Molecular Basis of Cardiovascular Diseases)

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16 pages, 4922 KiB

Open AccessArticle

Identification of Key Hypolipidemic Components and Exploration of the Potential Mechanism of Total Flavonoids from Rosa sterilis Based on Network Pharmacology, Molecular Docking, and Zebrafish Experiment

by Boxiao Wu, Churan Li, Xulu Luo, Huan Kan, Yonghe Li, Yingjun Zhang, Xiaoping Rao, Ping Zhao and Yun Liu

Curr. Issues Mol. Biol. 2024, 46(6), 5131-5146; https://doi.org/10.3390/cimb46060308 - 23 May 2024

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Abstract

Hyperlipidemia is a prevalent chronic metabolic disease that severely affects human health. Currently, commonly used clinical therapeutic drugs are prone to drug dependence and toxic side effects. Dietary intervention for treating chronic metabolic diseases has received widespread attention. Rosa sterilis is a characteristic fruit tree in China whose fruits are rich in flavonoids, which have been shown to have a therapeutic effect on hyperlipidemia; however, their exact molecular mechanism of action remains unclear. Therefore, this study aimed to investigate the therapeutic effects of R. sterilis total flavonoid extract (RS) on hyperlipidemia and its possible mechanisms. A hyperlipidemic zebrafish model was established using egg yolk powder and then treated with RS to observe changes in the integral optical density in the tail vessels. Network pharmacology and molecular docking were used to investigate the potential mechanism of action of RS for the treatment of hyperlipidemia. The results showed that RS exhibited favorable hypolipidemic effects on zebrafish in the concentration range of 3.0–30.0 μg/mL in a dose-dependent manner. Topological and molecular docking analyses identified HSP90AA1, PPARA, and MMP9 as key targets for hypolipidemic effects, which were exerted mainly through lipolytic regulation of adipocytes and lipids; pathway analysis revealed enrichment in atherosclerosis, chemical carcinogenic-receptor activation pathways in cancers, and proteoglycans in prostate cancer and other cancers. Mover, chinensinaphthol possessed higher content and better target binding ability, which suggested that chinensinaphthol might be an important component of RS with hypolipidemic active function. These findings provide a direction for further research on RS interventions for the treatment of hyperlipidemia. Full article

(This article belongs to the Special Issue A Focus on the Molecular Basis of Cardiovascular Diseases)

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18 pages, 2545 KiB

Open AccessReview

Cardiac Amyloidosis: State-of-the-Art Review in Molecular Pathology

by Cecilia Salzillo, Renato Franco, Andrea Ronchi, Andrea Quaranta and Andrea Marzullo

Curr. Issues Mol. Biol. 2024, 46(10), 11519-11536; https://doi.org/10.3390/cimb46100684 - 16 Oct 2024

Cited by 2 | Viewed by 4055

Abstract

Amyloidosis refers to a group of diseases caused by extracellular deposits of misfolded proteins, which alter tissue function and structure, potentially affecting any organ. The term “amyloid” was introduced in the 19th century and later associated with pathological protein deposits. Amyloid fibrils, which are insoluble and resistant to degradation, originate from soluble proteins that undergo misfolding. This process can be triggered by several factors, such as aging, elevated protein concentrations, or pathogenic variants. Amyloid deposits damage organs both by disrupting tissue architecture and through direct cytotoxic effects, leading to conditions such as heart failure. Amyloidosis can be classified into acquired or inherited forms and can be systemic or localized. Diagnosing cardiac amyloidosis is complex and often requires tissue biopsies, which are supported by Congo Red dye staining. In some cases, bisphosphonate bone scans may provide a less invasive diagnostic option. In this state-of-the-art review, we focus on the most common forms of cardiac amyloidosis, from epidemiology to therapy, emphasizing the differences in molecular mechanisms and the importance of pathological diagnosis for appropriate treatment using a multidisciplinary approach. Full article

(This article belongs to the Special Issue A Focus on the Molecular Basis of Cardiovascular Diseases)

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14 pages, 1217 KiB

Open AccessReview

Unraveling the Mechanisms of S100A8/A9 in Myocardial Injury and Dysfunction

by Yuanbo Xu, Yixuan Wang, Ke Ning and Yimin Bao

Curr. Issues Mol. Biol. 2024, 46(9), 9707-9720; https://doi.org/10.3390/cimb46090577 - 2 Sep 2024

Cited by 3 | Viewed by 1833

Abstract

S100A8 and S100A9, which are prominent members of the calcium-binding protein S100 family and recognized as calprotectin, form a robust heterodimer known as S100A8/A9, crucial for the manifestation of their diverse biological effects. Currently, there is a consensus that S100A8/A9 holds promise as a biomarker for cardiovascular diseases (CVDs), exerting an influence on cardiomyocytes or the cardiovascular system through multifaceted mechanisms that contribute to myocardial injury or dysfunction. In particular, the dualistic nature of S100A8/A9, which functions as both an inflammatory mediator and an anti-inflammatory agent, has garnered significantly increasing attention. This comprehensive review explores the intricate mechanisms through which S100A8/A9 operates in cardiovascular diseases, encompassing its bidirectional regulatory role in inflammation, the initiation of mitochondrial dysfunction, the dual modulation of myocardial fibrosis progression, and apoptosis and autophagy. The objective is to provide new information on and strategies for the clinical diagnosis and treatment of cardiovascular diseases in the future. Full article

(This article belongs to the Special Issue A Focus on the Molecular Basis of Cardiovascular Diseases)

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17 pages, 609 KiB

Open AccessReview

Recent Advances in Understanding the Molecular Mechanisms of SGLT2 Inhibitors in Atrial Remodeling

by Ioan-Alexandru Minciună, Raluca Tomoaia, Dragos Mihăilă, Gabriel Cismaru, Mihai Puiu, Radu Roșu, Gelu Simu, Florina Frîngu, Diana Andrada Irimie, Bogdan Caloian, Dumitru Zdrenghea and Dana Pop

Curr. Issues Mol. Biol. 2024, 46(9), 9607-9623; https://doi.org/10.3390/cimb46090571 - 31 Aug 2024

Cited by 1 | Viewed by 1780

Abstract

Atrial cardiomyopathy and remodeling play pivotal roles in the development of atrial fibrillation (AF) and heart failure (HF), involving complex changes in atrial structure and function. These changes facilitate the progression of AF and HF by creating a dynamic interplay between mechanical stress and electrical disturbances in the heart. Sodium–glucose cotransporter 2 inhibitors (SGLT2is), initially developed for the management of type 2 diabetes, have demonstrated promising cardiovascular benefits, being currently one of the cornerstone treatments in HF management. Despite recent data from randomized clinical trials indicating that SGLT2is may significantly influence atrial remodeling, their overall effectiveness in this context is still under debate. Given the emerging evidence, this review examines the molecular mechanisms through which SGLT2is exert their effects on atrial remodeling, aiming to clarify their potential benefits and limitations. By exploring these mechanisms, this review aims to provide insights into how SGLT2is can be integrated into strategies for preventing the progression of atrial remodeling and HF, as well as the development of AF. Full article

(This article belongs to the Special Issue A Focus on the Molecular Basis of Cardiovascular Diseases)

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21 pages, 1631 KiB

Open AccessReview

The Role of Alarmins in the Pathogenesis of Atherosclerosis and Myocardial Infarction

by Kajetan Kiełbowski, Patryk Skórka, Paulina Plewa, Estera Bakinowska and Andrzej Pawlik

Curr. Issues Mol. Biol. 2024, 46(8), 8995-9015; https://doi.org/10.3390/cimb46080532 - 17 Aug 2024

Cited by 1 | Viewed by 1949

Abstract

Atherosclerosis is a condition that is associated with lipid accumulation in the arterial intima. Consequently, the enlarging lesion, which is also known as an atherosclerotic plaque, may close the blood vessel lumen, thus leading to organ ischaemia. Furthermore, the plaque may rupture and initiate the formation of a thrombus, which can cause acute ischaemia. Atherosclerosis is a background pathological condition that can eventually lead to major cardiovascular diseases such as acute coronary syndrome or ischaemic stroke. The disorder is associated with an altered profile of alarmins, stress response molecules that are secreted due to cell injury or death and that induce inflammatory responses. High-mobility group box 1 (HMGB1), S100 proteins, interleukin-33, and heat shock proteins (HSPs) also affect the behaviour of endothelial cells and vascular smooth muscle cells (VSMCs). Thus, alarmins control the inflammatory responses of endothelial cells and proliferation of VSMCs, two important processes implicated in the pathogenesis of atherosclerosis. In this review, we will discuss the role of alarmins in the pathophysiology of atherosclerosis and myocardial infarction. Full article

(This article belongs to the Special Issue A Focus on the Molecular Basis of Cardiovascular Diseases)

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17 pages, 1367 KiB

Open AccessReview

Cardiovascular Risk in Philadelphia-Negative Myeloproliferative Neoplasms: Mechanisms and Implications—A Narrative Review

by Samuel Bogdan Todor, Cristian Ichim, Adrian Boicean and Romeo Gabriel Mihaila

Curr. Issues Mol. Biol. 2024, 46(8), 8407-8423; https://doi.org/10.3390/cimb46080496 - 2 Aug 2024

Cited by 19 | Viewed by 2092

Abstract

Myeloproliferative neoplasms (MPNs), encompassing disorders like polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF), are characterized by clonal hematopoiesis without the Philadelphia chromosome. The JAK2 V617F mutation is prevalent in PV, ET, and PMF, while mutations in MPL and CALR also play significant roles. These conditions predispose patients to thrombotic events, with PMF exhibiting the lowest survival among MPNs. Chronic inflammation, driven by cytokine release from aberrant leukocytes and platelets, amplifies cardiovascular risk through various mechanisms, including atherosclerosis and vascular remodeling. Additionally, MPN-related complications like pulmonary hypertension and cardiac fibrosis contribute to cardiovascular morbidity and mortality. This review consolidates recent research on MPNs’ cardiovascular implications, emphasizing thrombotic risk, chronic inflammation, and vascular stiffness. Understanding these associations is crucial for developing targeted therapies and improving outcomes in MPN patients. Full article

(This article belongs to the Special Issue A Focus on the Molecular Basis of Cardiovascular Diseases)

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13 pages, 731 KiB

Open AccessReview

The Evolving Role of Calcium Channel Blockers in Hypertension Management: Pharmacological and Clinical Considerations

by Kamryn E. Jones, Shaun L. Hayden, Hannah R. Meyer, Jillian L. Sandoz, William H. Arata, Kylie Dufrene, Corrado Ballaera, Yair Lopez Torres, Patricia Griffin, Adam M. Kaye, Sahar Shekoohi and Alan D. Kaye

Curr. Issues Mol. Biol. 2024, 46(7), 6315-6327; https://doi.org/10.3390/cimb46070377 - 22 Jun 2024

Cited by 8 | Viewed by 11984

Abstract

Worldwide, hypertension is the leading risk factor for cardiovascular disease and death. An estimated 122 million people, per the American Heart Association in 2023, have been diagnosed with this common condition. It is generally agreed that the primary goal in the treatment of hypertension is to reduce overall blood pressure to below 140/90 mmHg, with a more optimal goal of 130/80 mmHg. Common medications for treating hypertension include calcium channel blockers (CCBs), angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, beta-blockers, and diuretics. CCBs are one of the most widely studied agents and are generally recommended as first-line therapy alone and in combination therapies. This is largely based on the vast knowledge of CCB mechanisms and their minimal side effect profile. CCBs can be separated into two classes: dihydropyridine and non-dihydropyridine. Non-dihydropyridine CCBs act on voltage-dependent L-type calcium channels of cardiac and smooth muscle to decrease muscle contractility. Dihydropyridine CCBs act by vasodilating the peripheral vasculature. For many patients with only mild increases in systolic and diastolic blood pressure (e.g., stage 1 hypertension), the medical literature indicates that CCB monotherapy can be sufficient to control hypertension. In this regard, CCB monotherapy in those with stage 1 hypertension reduced renal and cardiovascular complications compared to other drug classes. Combination therapy with CCBs and angiotensin receptor blockers or angiotensin-converting enzyme inhibitors has been shown to be an effective dual therapy based on recent meta-analyses. This article is a review of calcium channel blockers and their use in treating hypertension with some updated and recent information on studies that have re-examined their use. As for new information, we tried to include some information from recent studies on hypertensive treatment involving calcium channel blockers. Full article

(This article belongs to the Special Issue A Focus on the Molecular Basis of Cardiovascular Diseases)

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