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Biomolecules
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Molecular Aspect of Cardiovascular Risk Factors
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Molecular Aspect of Cardiovascular Risk Factors

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Biological Factors".

Deadline for manuscript submissions: closed (28 February 2024) | Viewed by 20629

Special Issue Editors

Dr. Shang-Zhong Xu

E-Mail Website
Guest Editor
Centre for Atherothrombosis and Metabolic Disease, Hull York Medical School, University of Hull, Hull HU6 7RU, UK
Interests: cardiovascular disease; diabetic complications; obesity; osteoporosis; oxidative stress; Ca2+ signalling; ion channels; antioxidants; drug discovery
Prof. Dr. Thozhukat Sathyapalan

E-Mail Website
Guest Editor
Academic Endocrinology, Diabetes and Metabolism, Hull York Medical School, University of Hull, Hull HU6 7RU, UK
Interests: diabetes; obesity; nutrition; insulin resistance; glucose variability; polycystic ovary syndrome (PCOS); metabolic diseases; lipid metabolism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiovascular diseases (CVDs) are the leading cause of death globally, and 85% of CVD deaths are due to heart attacks and strokes. Understanding of the risk factors of CVDs and identification of their underlying molecular aspects is important for preventing CVDs.  There are a number of risk factors, including behavioural risk factors (unhealthy diet, physical inactivity, alcohol, and smoking), comorbidities (diabetes, obesity, hypertension, hyperlipidaemia, inflammation and infection), genetic variations, aging, and social risk factors (anxiety, psychological distress and poverty).

We are pleased to invite you to submit to this Special Issue on “Molecular Aspects of Cardiovascular Risk Factors”. This Special Issue aims to collect papers to reflect recent research and advances in cardiovascular risk factors and their various molecules and pathophysiological aspects in the disease processes.  We encourage contributions on molecular biology, biochemistry, physiology, and genetics to address diverse risk factors and their target proteins and signalling pathways.

In this Special Issue, original research articles and reviews are welcome. Research areas may include (but not be limited to) the following: biomarkers for risk factors; new target proteins; oxidative stress; mitochondrial dysfunction; homocysteine; ischaemic heart disease; vascular diseases; thrombosis; diabetes; obesity; diet supplements; antioxidants; exercise.

We look forward to receiving your contributions.

Dr. Shang-Zhong Xu
Prof. Dr. Thozhukat Sathyapalan
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. Biomolecules 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 2700 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

  • food drying
  • energy saving
  • food quality
  • traditional foodsdiabetic complications
  • obesity
  • hypertension
  • hyperlipidaemia
  • thrombosis
  • inflammation
  • diet
  • smoking
  • physical inactivity
  • hereditary factors
  • ageing

Published Papers (9 papers)

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Research

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16 pages, 4561 KiB  
Article
Activation of Cannabinoid Type 2 Receptor in Microglia Reduces Neuroinflammation through Inhibiting Aerobic Glycolysis to Relieve Hypertension
by Ruohan Shan, Yuxiang Zhang, Yiping Shi, Xiaowen Wang, Xueke Wang, Guanying Ma and Qian Li
Biomolecules 2024, 14(3), 333; https://doi.org/10.3390/biom14030333 - 11 Mar 2024
Viewed by 879
Abstract
Background: Studies have shown that the chronic use of cannabis is associated with a decrease in blood pressure. Our previous studies prove that activating the cannabinoid type 2 (CB2) receptor in the brain can effectively reduce blood pressure in spontaneously hypertensive rats; however, [...] Read more.
Background: Studies have shown that the chronic use of cannabis is associated with a decrease in blood pressure. Our previous studies prove that activating the cannabinoid type 2 (CB2) receptor in the brain can effectively reduce blood pressure in spontaneously hypertensive rats; however, the exact mechanism has not been clarified. The objective of this study is to demonstrate that activation of microglial CB2 receptors can effectively reduce the levels of TNF-α, IL-1β, and IL-6 in the paraventricular nucleus (PVN) through inhibiting aerobic glycolysis, thereby relieving hypertension. Methods: AngiotensinII (AngII) was administered to BV2 cells and C57 mice to induce hypertension and the release of proinflammatory cytokines. The mRNA and protein expression of the CB2 receptor, TNF-α, IL-1β, IL-6, and the PFK and LDHa enzymes were detected using RT-qPCR and Western blotting. The Seahorse XF Energy Metabolism Analyzer was used to measure the oxidative phosphorylation and aerobic glycolysis metabolic pathways in BV2 cells. The long-term effects of injecting JWH133, a selective CB2 receptor agonist, intraperitoneally on blood pressure were ascertained. ELISA was used to measure norepinephrine and lactic acid levels while immunofluorescence labeling was used to locate the CB2 receptor and c-Fos. By injecting pAAV-F4/80-GFP-mir30shRNA (AAV2-r-CB2shRNA) into the lateral cerebral ventricle, the CB2 receptor in microglia was specifically knocked down. Results: Activation of CB2 receptors by the agonist JWH133 suppressed TNF-α, IL-1β, and IL-6 by inhibiting PFK and LDHa enzymes involved in glycolysis, as well as lactic acid accumulation, along with a reduction in glycoPER levels (marks of aerobic glycolysis) in AngII-treated BV2 cells. In AngII-treated mice, the administration of JWH133 specifically activated CB2 receptors on microglia, resulting in decreased expression levels of PFK, LDHa, TNF-α, IL-1β, and IL-6, subsequently leading to a decrease in c-Fos protein expression within PVN neurons as well as reduced norepinephrine levels in plasma, ultimately contributing to blood pressure reduction. Conclusion: The results suggest that activation of the microglia CB2 receptor decreases the neuroinflammation to relieve hypertension; the underlying mechanism is related to inhibiting aerobic glycolysis of microglia. Full article
(This article belongs to the Special Issue Molecular Aspect of Cardiovascular Risk Factors)
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15 pages, 2404 KiB  
Article
High Phosphate-Induced JAK-STAT Signalling Sustains Vascular Smooth Muscle Cell Inflammation and Limits Calcification
by Federica Macrì, Ilaria Vigorito, Stefania Castiglione, Stefano Faggiano, Manuel Casaburo, Nadia Fanotti, Luca Piacentini, Davide Vigetti, Maria Cristina Vinci and Angela Raucci
Biomolecules 2024, 14(1), 29; https://doi.org/10.3390/biom14010029 - 24 Dec 2023
Viewed by 1616
Abstract
Vascular calcification (VC) is an age-related complication characterised by calcium-phosphate deposition in the arterial wall driven by the osteogenic transformation of vascular smooth muscle cells (VSMCs). The JAK-STAT pathway is an emerging target in inflammation. Considering the relationship between VC and inflammation, we [...] Read more.
Vascular calcification (VC) is an age-related complication characterised by calcium-phosphate deposition in the arterial wall driven by the osteogenic transformation of vascular smooth muscle cells (VSMCs). The JAK-STAT pathway is an emerging target in inflammation. Considering the relationship between VC and inflammation, we investigated the role of JAK-STAT signalling during VSMC calcification. Human aortic smooth muscle cells (HASMCs) were cultured in high-inorganic phosphate (Pi) medium for up to 7 days; calcium deposition was determined via Alizarin staining and colorimetric assay. Inflammatory factor secretion was evaluated via ELISA and JAK-STAT members’ activation using Western blot or immunohistochemistry on HASMCs or calcified aortas of Vitamin D-treated C57BL6/J mice, respectively. The JAK-STAT pathway was blocked by JAK Inhibitor I and Von Kossa staining was used for calcium deposits in murine aortic rings. During Pi-induced calcification, HASMCs released IL-6, IL-8, and MCP-1 and activated JAK1-JAK3 proteins and STAT1. Phospho-STAT1 was detected in murine calcified aortas. Blocking of the JAK-STAT cascade reduced HASMC proliferation and pro-inflammatory factor expression and release while increasing calcium deposition and osteogenic transcription factor RUNX2 expression. Consistently, JAK-STAT pathway inhibition exacerbates mouse aortic ring calcification ex vivo. Intriguingly, our results suggest an alternative link between VSMC inflammation and VC. Full article
(This article belongs to the Special Issue Molecular Aspect of Cardiovascular Risk Factors)
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16 pages, 3898 KiB  
Article
Ca2+ Influx through TRPC Channels Is Regulated by Homocysteine–Copper Complexes
by Gui-Lan Chen, Bo Zeng, Hongni Jiang, Nikoleta Daskoulidou, Rahul Saurabh, Rumbidzai J. Chitando and Shang-Zhong Xu
Biomolecules 2023, 13(6), 952; https://doi.org/10.3390/biom13060952 - 06 Jun 2023
Viewed by 1364
Abstract
An elevated level of circulating homocysteine (Hcy) has been regarded as an independent risk factor for cardiovascular disease; however, the clinical benefit of Hcy lowering-therapy is not satisfying. To explore potential unrevealed mechanisms, we investigated the roles of Ca2+ influx through TRPC [...] Read more.
An elevated level of circulating homocysteine (Hcy) has been regarded as an independent risk factor for cardiovascular disease; however, the clinical benefit of Hcy lowering-therapy is not satisfying. To explore potential unrevealed mechanisms, we investigated the roles of Ca2+ influx through TRPC channels and regulation by Hcy–copper complexes. Using primary cultured human aortic endothelial cells and HEK-293 T-REx cells with inducible TRPC gene expression, we found that Hcy increased the Ca2+ influx in vascular endothelial cells through the activation of TRPC4 and TRPC5. The activity of TRPC4 and TRPC5 was regulated by extracellular divalent copper (Cu2+) and Hcy. Hcy prevented channel activation by divalent copper, but monovalent copper (Cu+) had no effect on the TRPC channels. The glutamic acids (E542/E543) and the cysteine residue (C554) in the extracellular pore region of the TRPC4 channel mediated the effect of Hcy–copper complexes. The interaction of Hcy–copper significantly regulated endothelial proliferation, migration, and angiogenesis. Our results suggest that Hcy–copper complexes function as a new pair of endogenous regulators for TRPC channel activity. This finding gives a new understanding of the pathogenesis of hyperhomocysteinemia and may explain the unsatisfying clinical outcome of Hcy-lowering therapy and the potential benefit of copper-chelating therapy. Full article
(This article belongs to the Special Issue Molecular Aspect of Cardiovascular Risk Factors)
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Review

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25 pages, 4258 KiB  
Review
Biomarkers in Peripartum Cardiomyopathy—What We Know and What Is Still to Be Found
by Karolina E. Kryczka, Marcin Demkow and Zofia Dzielińska
Biomolecules 2024, 14(1), 103; https://doi.org/10.3390/biom14010103 - 12 Jan 2024
Viewed by 1446
Abstract
Peripartum cardiomyopathy (PPCM) is a form of heart failure, often severe, that occurs in previously healthy women at the end of their pregnancy or in the first few months after delivery. In PPCM, the recovery of heart function reaches 45–50%. However, the all-cause [...] Read more.
Peripartum cardiomyopathy (PPCM) is a form of heart failure, often severe, that occurs in previously healthy women at the end of their pregnancy or in the first few months after delivery. In PPCM, the recovery of heart function reaches 45–50%. However, the all-cause mortality in long-term observation remains high, reaching 20% irrespective of recovery status. The incidence of PPCM is increasing globally; therefore, effort is required to clarify the pathophysiological background of the disease, as well as to discover specific diagnostic and prognostic biomarkers. The etiology of the disease remains unclear, including oxidative stress; inflammation; hormonal disturbances; endothelial, microcirculatory, cardiomyocyte and extracellular matrix dysfunction; fibrosis; and genetic mutations. Currently, antiangiogenic 16-kDa prolactin (PRL), cleaved from standard 23-kDa PRL in the case of unbalanced oxidative stress, is recognized as the main trigger of the disease. In addition, 16-kDa PRL causes damage to cardiomyocytes, acting via microRNA-146a secreted from endothelial cells as a cause of the NF-κβ pathway. Bromocriptine, which inhibits the secretion of PRL from the pituitary gland, is now the only specific treatment for PPCM. Many different phenotypes of the disease, as well as cases of non-responders to bromocriptine treatment, indicate other pathophysiological pathways that need further investigation. Biomarkers in PPCM are not well established. There is a deficiency in specific diagnostic biomarkers. Pro-brain-type natriuretic peptide (BNP) and N-terminal BNP are the best, however unspecific, diagnostic biomarkers of heart failure at the moment. Therefore, more efforts should be engaged in investigating more specific biomolecules of a diagnostic and prognostic manner such as 16-kDa PRL, galectin-3, myeloperoxidase, or soluble Fms-like tyrosine kinase-1/placental growth factor ratio. In this review, we present the current state of knowledge and future directions of exploring PPCM pathophysiology, including microRNA and heat shock proteins, which may improve diagnosis, treatment monitoring, and the development of specific treatment strategies, and consequently improve patients’ prognosis and outcome. Full article
(This article belongs to the Special Issue Molecular Aspect of Cardiovascular Risk Factors)
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11 pages, 252 KiB  
Review
Should Cystatin C eGFR Become Routine Clinical Practice?
by Sebastian Spencer, Robert Desborough and Sunil Bhandari
Biomolecules 2023, 13(7), 1075; https://doi.org/10.3390/biom13071075 - 05 Jul 2023
Cited by 3 | Viewed by 2535
Abstract
Kidney function assessment is crucial for diagnosing and managing kidney diseases. Glomerular filtration rate (GFR) is widely used as an indicator of kidney function, but its direct measurement is challenging. Serum creatinine, a commonly used marker for estimating GFR (eGFR), has limitations in [...] Read more.
Kidney function assessment is crucial for diagnosing and managing kidney diseases. Glomerular filtration rate (GFR) is widely used as an indicator of kidney function, but its direct measurement is challenging. Serum creatinine, a commonly used marker for estimating GFR (eGFR), has limitations in accuracy and sensitivity. Cystatin C, a protein freely filtered by the glomerulus, has emerged as a promising alternative marker for kidney function. It is unaffected by muscle mass and shows stronger associations with cardiovascular disease and mortality than creatinine. Various equations have been developed to estimate GFR using creatinine or cystatin C alone or in combination. The CKD-EPIcreat-cys equation combining both markers demonstrates improved accuracy in GFR estimation, especially for individuals with eGFR values of 45–59 mL/min/1.73 m2. Cystatin C-based estimates of GFR outperform creatinine-based estimates in predicting clinical outcomes and identifying patients at higher risk, particularly in elderly and non-white ethnic groups. Cystatin C offers advantages over creatinine as a marker of kidney function. It is not influenced by non-kidney factors and provides more accurate estimation of GFR, aiding in the early detection of kidney disease and predicting adverse outcomes. Incorporating cystatin C into routine kidney function assessment may improve patient risk stratification and guide clinical decision-making. However, widespread adoption of cystatin C testing requires increased availability and accessibility in clinical laboratories. Further research and implementation efforts are needed to fully realize the potential of cystatin C in kidney function assessment and improving patient outcomes. Full article
(This article belongs to the Special Issue Molecular Aspect of Cardiovascular Risk Factors)
17 pages, 1356 KiB  
Review
Aldosterone: Essential for Life but Damaging to the Vascular Endothelium
by Michael Crompton, Laura J. Skinner, Simon C. Satchell and Matthew J. Butler
Biomolecules 2023, 13(6), 1004; https://doi.org/10.3390/biom13061004 - 17 Jun 2023
Cited by 3 | Viewed by 3277
Abstract
The renin angiotensin aldosterone system is a key regulator of blood pressure. Aldosterone is the final effector of this pathway, acting predominantly via mineralocorticoid receptors. Aldosterone facilitates the conservation of sodium and, with it, water and acts as a powerful stimulus for potassium [...] Read more.
The renin angiotensin aldosterone system is a key regulator of blood pressure. Aldosterone is the final effector of this pathway, acting predominantly via mineralocorticoid receptors. Aldosterone facilitates the conservation of sodium and, with it, water and acts as a powerful stimulus for potassium excretion. However, evidence for the pathological impact of excess mineralocorticoid receptor stimulation is increasing. Here, we discussed how in the heart, hyperaldosteronism is associated with fibrosis, cardiac dysfunction, and maladaptive hypertrophy. In the kidney, aldosterone was shown to cause proteinuria and fibrosis and may contribute to the progression of kidney disease. More recently, studies suggested that aldosterone excess damaged endothelial cells. Here, we reviewed how damage to the endothelial glycocalyx may contribute to this process. The endothelial glycocalyx is a heterogenous, negatively charged layer on the luminal surface of cells. Aldosterone exposure alters this layer. The resulting structural changes reduced endothelial reactivity in response to protective shear stress, altered permeability, and increased immune cell trafficking. Finally, we reviewed current therapeutic strategies for limiting endothelial damage and suggested that preventing glycocalyx remodelling in response to aldosterone exposure may provide a novel strategy, free from the serious adverse effect of hyperkalaemia seen in response to mineralocorticoid blockade. Full article
(This article belongs to the Special Issue Molecular Aspect of Cardiovascular Risk Factors)
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14 pages, 1691 KiB  
Review
Sphingosine-1-Phosphate Signaling in Cardiovascular Diseases
by Na Wang, Jing-Yi Li, Bo Zeng and Gui-Lan Chen
Biomolecules 2023, 13(5), 818; https://doi.org/10.3390/biom13050818 - 11 May 2023
Cited by 3 | Viewed by 2533
Abstract
Sphingosine-1-phosphate (S1P) is an important sphingolipid molecule involved in regulating cardiovascular functions in physiological and pathological conditions by binding and activating the three G protein-coupled receptors (S1PR1, S1PR2, and S1PR3) expressed in endothelial and smooth muscle cells, as well as cardiomyocytes and fibroblasts. [...] Read more.
Sphingosine-1-phosphate (S1P) is an important sphingolipid molecule involved in regulating cardiovascular functions in physiological and pathological conditions by binding and activating the three G protein-coupled receptors (S1PR1, S1PR2, and S1PR3) expressed in endothelial and smooth muscle cells, as well as cardiomyocytes and fibroblasts. It exerts its actions through various downstream signaling pathways mediating cell proliferation, migration, differentiation, and apoptosis. S1P is essential for the development of the cardiovascular system, and abnormal S1P content in the circulation is involved in the pathogenesis of cardiovascular disorders. This article reviews the effects of S1P on cardiovascular function and signaling mechanisms in different cell types in the heart and blood vessels under diseased conditions. Finally, we look forward to more clinical findings with approved S1PR modulators and the development of S1P-based therapies for cardiovascular diseases. Full article
(This article belongs to the Special Issue Molecular Aspect of Cardiovascular Risk Factors)
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19 pages, 4583 KiB  
Review
Restoring Epigenetic Reprogramming with Diet and Exercise to Improve Health-Related Metabolic Diseases
by Merlin Jesso Abraham, Adham El Sherbini, Mohammad El-Diasty, Sussan Askari and Myron R. Szewczuk
Biomolecules 2023, 13(2), 318; https://doi.org/10.3390/biom13020318 - 07 Feb 2023
Cited by 3 | Viewed by 3174
Abstract
Epigenetic reprogramming predicts the long-term functional health effects of health-related metabolic disease. This epigenetic reprogramming is activated by exogenous or endogenous insults, leading to altered healthy and different disease states. The epigenetic and environmental changes involve a roadmap of epigenetic networking, such as [...] Read more.
Epigenetic reprogramming predicts the long-term functional health effects of health-related metabolic disease. This epigenetic reprogramming is activated by exogenous or endogenous insults, leading to altered healthy and different disease states. The epigenetic and environmental changes involve a roadmap of epigenetic networking, such as dietary components and exercise on epigenetic imprinting and restoring epigenome patterns laid down during embryonic development, which are paramount to establishing youthful cell type and health. Nutrition and exercise are among the most well-known environmental epigenetic factors influencing the proper developmental and functional lifestyle, with potential beneficial or detrimental effects on health status. The diet and exercise strategies applied from conception could represent an innovative epigenetic target for preventing and treating human diseases. Here, we describe the potential role of diet and exercise as therapeutic epigenetic strategies for health and diseases, highlighting putative future perspectives in this field. Full article
(This article belongs to the Special Issue Molecular Aspect of Cardiovascular Risk Factors)
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18 pages, 1828 KiB  
Review
The Role of Platelets in Hypoglycemia-Induced Cardiovascular Disease: A Review of the Literature
by Ahmed Ali Gebril Ali, Sara Anjum Niinuma, Abu Saleh Md Moin, Stephen L. Atkin and Alexandra E. Butler
Biomolecules 2023, 13(2), 241; https://doi.org/10.3390/biom13020241 - 27 Jan 2023
Cited by 1 | Viewed by 2629
Abstract
Cardiovascular diseases (CVDs) are the leading cause of death globally as well as the leading cause of mortality and morbidity in type 2 diabetes (T2D) patients. Results from large interventional studies have suggested hyperglycemia and poor glycemic control to be largely responsible for [...] Read more.
Cardiovascular diseases (CVDs) are the leading cause of death globally as well as the leading cause of mortality and morbidity in type 2 diabetes (T2D) patients. Results from large interventional studies have suggested hyperglycemia and poor glycemic control to be largely responsible for the development of CVDs. However, the association between hypoglycemia and cardiovascular events is also a key pathophysiological factor in the development of CVDs. Hypoglycemia is especially prevalent in T2D patients treated with oral sulfonylurea agents or exogenous insulin, increasing the susceptibility of this population to cardiovascular events. The adverse cardiovascular risk of hypoglycemia can persist even after the blood glucose levels have been normalized. Hypoglycemia may lead to vascular disease through mechanisms such as enhanced coagulation, oxidative stress, vascular inflammation, endothelial dysfunction, and platelet activation. In the following review, we summarize the evidence for the role of hypoglycemia in platelet activation and the subsequent effects this may have on the development of CVD. In addition, we review current evidence for the effectiveness of therapies in reducing the risk of CVDs. Full article
(This article belongs to the Special Issue Molecular Aspect of Cardiovascular Risk Factors)
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