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New Trends in Diabetes, Hypertension and Cardiovascular Diseases: 3rd Edition
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New Trends in Diabetes, Hypertension and Cardiovascular Diseases: 3rd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 July 2025 | Viewed by 11299

Special Issue Editors

Dr. Yutang Wang

E-Mail Website
Guest Editor
Discipline of Life Science, Institute of Innovation, Science and Sustainability, Federation University Australia, Ballarat, VIC 3350, Australia
Interests: cardiovascular disease; hypertension; diabetes; atherosclerosis; abdominal aortic aneurysm; renal denervation; dyslipidemia; hyperuricemia
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Dianna Magliano

E-Mail Website
Guest Editor
1. School of Public Health and Preventive Medicine, Monash University, Melbourne, VIC 3004, Australia
2. Baker Heart and Diabetes Institute, Melbourne, VIC 3004, Australia
Interests: diabetes; obesity; population health
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is a continuation of our previous successful Special Issue “New Trends in Diabetes, Hypertension and Cardiovascular Diseases 2.0” (https://www.mdpi.com/journal/ijms/special_issues/W2U51NUN39).

Cardiovascular disease (CVD) is the leading cause of death worldwide, representing one-third of all global deaths. Comorbidities such as hypertension and diabetes will significantly increase the risk of cardiovascular events and mortality. Breakthroughs in cardiovascular research and medicine have led to a decrease in cardiovascular morbidity and mortality. However, more research is needed to further understand the molecular mechanism of hypertension, diabetes, and CVD which could eventually help to reduce the CVD burden. This Special Issue of IJMS will cover the latest developments in pathogenesis and the molecular mechanisms underlying hypertension, diabetes, and CVD (such as myocardial infarction and stroke), as well as molecular mechanisms underlying therapeutic and other types of treatments against CVD.

Dr. Yutang Wang
Prof. Dr. Dianna Magliano
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 disease
  • myocardial infarction
  • stroke
  • transient ischaemic attack
  • hypertension
  • diabetes mellitus
  • atherosclerosis
  • inflammation

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Related Special Issues

Published Papers (5 papers)

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Research

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16 pages, 1798 KiB  
Article
Low-Dose Docetaxel Is Effective in Reducing Atherogenic Lipids and Atherosclerosis
by Hong Y. Choi, Isabelle Ruel, Shiwon Choi, Iulia Iatan, Senna Choi, Jyh-Yeuan Lee and Jacques Genest
Int. J. Mol. Sci. 2025, 26(4), 1484; https://doi.org/10.3390/ijms26041484 - 11 Feb 2025
Viewed by 708
Abstract
High-density lipoprotein (HDL) particles form during cellular cholesterol removal, positioning HDL biogenesis as a potential strategy to combat atherosclerosis. We identified desmocollin 1 (DSC1) as a negative regulator of HDL biogenesis and discovered that docetaxel (DTX) effectively inhibits DSC1 activity. This study assessed [...] Read more.
High-density lipoprotein (HDL) particles form during cellular cholesterol removal, positioning HDL biogenesis as a potential strategy to combat atherosclerosis. We identified desmocollin 1 (DSC1) as a negative regulator of HDL biogenesis and discovered that docetaxel (DTX) effectively inhibits DSC1 activity. This study assessed the efficacy of DTX in reducing atherosclerosis in ApoE−/− mice. After two weeks on a high-fat diet, mice were divided into baseline, vehicle-treated, and DTX-treated groups. Baseline mice were sacrificed at the end of the two weeks, while the other groups received a vehicle or DTX (1 μg/μL) via subcutaneously implanted osmotic pumps delivering 0.15 μL/h for six weeks, with the high-fat diet continued. The controlled drug delivery system maintained stable DTX blood concentrations (2.7–4.3 nM) over six weeks without hematologic toxicity. DTX treatment significantly reduced circulating atherogenic lipids, including triglycerides, non-esterified fatty acids, low-density lipoprotein cholesterol, and total cholesterol, while increasing the HDL cholesterol/total cholesterol ratio. These improvements were associated with significant reductions in atherosclerotic lesions in the aortic sinus and arch. Notably, these effects occurred without altering circulating inflammatory cytokine levels. These results demonstrate that DTX effectively reduces dyslipidemia-induced atherosclerosis. Its HDL-biogenic and anti-atherosclerotic effects establish DTX as a promising candidate for developing HDL-directed therapies for atherosclerosis. Full article
(This article belongs to the Special Issue New Trends in Diabetes, Hypertension and Cardiovascular Diseases: 3rd Edition)
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15 pages, 1404 KiB  
Article
The Genetic Variants Influencing Hypertension Prevalence Based on the Risk of Insulin Resistance as Assessed Using the Metabolic Score for Insulin Resistance (METS-IR)
by Bo-Kyung Shine, Ja-Eun Choi, Young-Jin Park and Kyung-Won Hong
Int. J. Mol. Sci. 2024, 25(23), 12690; https://doi.org/10.3390/ijms252312690 - 26 Nov 2024
Cited by 1 | Viewed by 1052
Abstract
Insulin resistance is a major indicator of cardiovascular diseases, including hypertension. The Metabolic Score for Insulin Resistance (METS-IR) offers a simplified and cost-effective way to evaluate insulin resistance. This study aimed to identify genetic variants associated with the prevalence of hypertension stratified by [...] Read more.
Insulin resistance is a major indicator of cardiovascular diseases, including hypertension. The Metabolic Score for Insulin Resistance (METS-IR) offers a simplified and cost-effective way to evaluate insulin resistance. This study aimed to identify genetic variants associated with the prevalence of hypertension stratified by METS-IR score levels. Data from the Korean Genome and Epidemiology Study (KoGES) were analyzed. The METS-IR was calculated using the following formula: ln [(2 × fasting blood glucose (FBG) + triglycerides (TG)) × body mass index (BMI)]/ ln [high-density lipoprotein cholesterol (HDL-C)]. The participants were divided into tertiles 1 (T1) and 3 (T3) based on their METS-IR scores. Genome-wide association studies (GWAS) were performed for hypertensive cases and non-hypertensive controls within these tertile groups using logistic regression adjusted for age, sex, and lifestyle factors. Among the METS-IR tertile groups, 3517 of the 19,774 participants (17.8%) at T1 had hypertension, whereas 8653 of the 20,374 participants (42.5%) at T3 had hypertension. A total of 113 single-nucleotide polymorphisms (SNPs) reached the GWAS significance threshold (p < 5 × 10−8) in at least one tertile group, mapping to six distinct genetic loci. Notably, four loci, rs11899121 (chr2p24), rs7556898 (chr2q24.3), rs17249754 (ATP2B1), and rs1980854 (chr20p12.2), were significantly associated with hypertension in the high-METS-score group (T3). rs10857147 (FGF5) was significant in both the T1 and T3 groups, whereas rs671 (ALDH2) was significant only in the T1 group. The GWASs identified six genetic loci significantly associated with hypertension, with distinct patterns across METS-IR tertiles, highlighting the role of metabolic context in genetic susceptibility. These findings underscore critical genetic factors influencing hypertension prevalence and provide insights into the metabolic–genetic interplay underlying this condition. Full article
(This article belongs to the Special Issue New Trends in Diabetes, Hypertension and Cardiovascular Diseases: 3rd Edition)
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24 pages, 4250 KiB  
Article
Gut Microbiota and Metabolic Alterations Associated with Heart Failure and Coronary Artery Disease
by Adel A. Yafarova, Elena V. Dementeva, Olga A. Zlobovskaya, Anna F. Sheptulina, Elena V. Lopatukhina, Yuriy S. Timofeev, Evgeniya V. Glazunova, Aleksey V. Lyundup, Yuriy V. Doludin, Anton R. Kiselev, German A. Shipulin, Valentin V. Makarov, Oxana M. Drapkina and Sergey M. Yudin
Int. J. Mol. Sci. 2024, 25(20), 11295; https://doi.org/10.3390/ijms252011295 - 20 Oct 2024
Cited by 3 | Viewed by 2856
Abstract
This study investigates the role of gut microbiota in cardiovascular diseases, with an additional focus on pro-atherogenic metabolites. We use advanced network analysis and machine learning techniques to identify key microbial features linked to coronary artery disease (CAD) and heart failure with reduced [...] Read more.
This study investigates the role of gut microbiota in cardiovascular diseases, with an additional focus on pro-atherogenic metabolites. We use advanced network analysis and machine learning techniques to identify key microbial features linked to coronary artery disease (CAD) and heart failure with reduced ejection fraction (HFrEF). This cross-sectional study included 189 participants divided into three groups: coronary artery disease (n = 93), heart failure with reduced ejection fraction (n = 43), and controls (n = 53). Assessments included physical exams, echocardiography, dietary surveys, blood analysis, and fecal analysis. Gut microbiota composition was analyzed using next-generation sequencing (NGS) and quantitative polymerase chain reaction (qPCR). Statistical analysis methods for testing hypotheses and correlations, alpha and beta-diversity analyses, co-occurrence networks, and machine learning were conducted using Python libraries or R packages with multiple comparisons corrected using the Benjamini–Hochberg procedure. Significant gut microbiota alterations were observed, with higher Bacillota/Bacteroidota ratios in CAD and HFrEF groups compared to controls (p < 0.001). Significant differences were observed in α-diversity indices (Pielou, Chao1, Faith) between disease groups and controls (p < 0.001). β-diversity analyses also revealed distinct microbial profiles (p = 0.0015). Interestingly, trimethylamine N-oxide (TMAO) levels were lower in CAD and HFrEF groups compared to controls (p < 0.05), while indoxyl sulfate (IS) levels were comparable between the study groups. Co-occurrence network analysis and machine learning identified key microbial features linked to these conditions, highlighting complex interactions within the gut microbiota associated with cardiovascular disease. Full article
(This article belongs to the Special Issue New Trends in Diabetes, Hypertension and Cardiovascular Diseases: 3rd Edition)
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Review

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30 pages, 5310 KiB  
Review
From DNA Repair to Redox Signaling: The Multifaceted Role of APEX1 (Apurinic/Apyrimidinic Endonuclease 1) in Cardiovascular Health and Disease
by Huan-Huan Yuan, Hao Yin, Mara Marincas, Ling-Li Xie, Lan-Lan Bu, Min-Hua Guo and Xi-Long Zheng
Int. J. Mol. Sci. 2025, 26(7), 3034; https://doi.org/10.3390/ijms26073034 - 26 Mar 2025
Viewed by 560
Abstract
Apurinic/apyrimidinic endonuclease 1 (APEX1) serves as a potent regulatory factor in innate immunity, exhibiting both redox and endonuclease activities. Its redox function enables the regulation of transcription factors such as NF-κB or STAT3, whereas its endonuclease activity recognizes apurinic/apyrimidinic (AP) sites in damaged [...] Read more.
Apurinic/apyrimidinic endonuclease 1 (APEX1) serves as a potent regulatory factor in innate immunity, exhibiting both redox and endonuclease activities. Its redox function enables the regulation of transcription factors such as NF-κB or STAT3, whereas its endonuclease activity recognizes apurinic/apyrimidinic (AP) sites in damaged DNA lesions during base excision repair (BER) and double-stranded DNA repair, thereby I confirm.anti-inflammatory, antioxidative stress and antiapoptotic effects. APEX1 is expressed in a variety of cell types that constitute the cardiovascular system, including cardiomyocytes, endothelial cells, smooth muscle cells, and immune cells. Emerging genetic and experimental evidence points towards the functional roles of APEX1 in the pathophysiology of cardiovascular diseases, including neointimal formation and atherosclerosis. This review aims to present comprehensive coverage of the up-to-date literature concerning the molecular and cellular functions of APEX1, with a particular focus on how APEX1 contributes to the (dys)functions of different cell types during the pathogenesis of cardiovascular diseases. Furthermore, we underscore the potential of APEX1 as a therapeutic target for the treatment of cardiovascular diseases. Full article
(This article belongs to the Special Issue New Trends in Diabetes, Hypertension and Cardiovascular Diseases: 3rd Edition)
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40 pages, 10508 KiB  
Review
Neuroimmune Interactions and Their Role in Immune Cell Trafficking in Cardiovascular Diseases and Cancer
by Yutang Wang, Jack C. Anesi, Indu S. Panicker, Darcy Cook, Prapti Bista, Yan Fang and Ernesto Oqueli
Int. J. Mol. Sci. 2025, 26(6), 2553; https://doi.org/10.3390/ijms26062553 - 12 Mar 2025
Viewed by 872
Abstract
Sympathetic nerves innervate bone marrow and various immune organs, where norepinephrine—the primary sympathetic neurotransmitter—directly interacts with immune cells that express adrenergic receptors. This article reviewed the key molecular pathways triggered by sympathetic activation and explored how sympathetic activity influences immune cell migration. Norepinephrine [...] Read more.
Sympathetic nerves innervate bone marrow and various immune organs, where norepinephrine—the primary sympathetic neurotransmitter—directly interacts with immune cells that express adrenergic receptors. This article reviewed the key molecular pathways triggered by sympathetic activation and explored how sympathetic activity influences immune cell migration. Norepinephrine serves as a chemoattractant for monocytes, macrophages, and stem cells, promoting the migration of myeloid cells while inhibiting the migration of lymphocytes at physiological concentrations. We also examined the role of immune cell infiltration in cardiovascular diseases and cancer. Evidence suggests that sympathetic activation increases myeloid cell infiltration into target tissues across various cardiovascular diseases, including atherosclerosis, hypertension, cardiac fibrosis, cardiac hypertrophy, arrhythmia, myocardial infarction, heart failure, and stroke. Conversely, inhibiting sympathetic activity may serve as a potential therapeutic strategy to treat these conditions by reducing macrophage infiltration. Furthermore, sympathetic activation promotes macrophage accumulation in cancer tissues, mirroring its effects in cardiovascular diseases, while suppressing T lymphocyte infiltration into cancerous sites. These changes contribute to increased cancer growth and metastasis. Thus, inhibiting sympathetic activation could help to protect against cancer by enhancing T cell infiltration and reducing macrophage presence in tumors. Full article
(This article belongs to the Special Issue New Trends in Diabetes, Hypertension and Cardiovascular Diseases: 3rd Edition)
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