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New Trends in Diabetes, Hypertension and Cardiovascular Diseases 2.0

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: 30 May 2024 | Viewed by 7213

Special Issue Editors

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
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".

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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Published Papers (5 papers)

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Research

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43 pages, 8752 KiB  
Article
T-Cell Receptor Sequences Identify Combined Coxsackievirus–Streptococci Infections as Triggers for Autoimmune Myocarditis and Coxsackievirus–Clostridia Infections for Type 1 Diabetes
Int. J. Mol. Sci. 2024, 25(3), 1797; https://doi.org/10.3390/ijms25031797 - 01 Feb 2024
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Abstract
Recent research suggests that T-cell receptor (TCR) sequences expanded during human immunodeficiency virus and SARS-CoV-2 infections unexpectedly mimic these viruses. The hypothesis tested here is that TCR sequences expanded in patients with type 1 diabetes mellitus (T1DM) and autoimmune myocarditis (AM) mimic the [...] Read more.
Recent research suggests that T-cell receptor (TCR) sequences expanded during human immunodeficiency virus and SARS-CoV-2 infections unexpectedly mimic these viruses. The hypothesis tested here is that TCR sequences expanded in patients with type 1 diabetes mellitus (T1DM) and autoimmune myocarditis (AM) mimic the infectious triggers of these diseases. Indeed, TCR sequences mimicking coxsackieviruses, which are implicated as triggers of both diseases, are statistically significantly increased in both T1DM and AM patients. However, TCRs mimicking Clostridia antigens are significantly expanded in T1DM, whereas TCRs mimicking Streptococcal antigens are expanded in AM. Notably, Clostridia antigens mimic T1DM autoantigens, such as insulin and glutamic acid decarboxylase, whereas Streptococcal antigens mimic cardiac autoantigens, such as myosin and laminins. Thus, T1DM may be triggered by combined infections of coxsackieviruses with Clostridia bacteria, while AM may be triggered by coxsackieviruses with Streptococci. These TCR results are consistent with both epidemiological and clinical data and recent experimental studies of cross-reactivities of coxsackievirus, Clostridial, and Streptococcal antibodies with T1DM and AM antigens. These data provide the basis for developing novel animal models of AM and T1DM and may provide a generalizable method for revealing the etiologies of other autoimmune diseases. Theories to explain these results are explored. Full article
(This article belongs to the Special Issue New Trends in Diabetes, Hypertension and Cardiovascular Diseases 2.0)
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13 pages, 3547 KiB  
Article
Does Hypertension Affect the Recovery of Renal Functions after Reversal of Unilateral Ureteric Obstruction?
Int. J. Mol. Sci. 2024, 25(3), 1540; https://doi.org/10.3390/ijms25031540 - 26 Jan 2024
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Abstract
Research has demonstrated that hypertension can lead to an exaggeration in the renal functional and histological changes caused by ureteral obstruction. These changes were particularly observed shortly after the release of a relatively brief period of unilateral ureteral obstruction (UUO). However, the long-term [...] Read more.
Research has demonstrated that hypertension can lead to an exaggeration in the renal functional and histological changes caused by ureteral obstruction. These changes were particularly observed shortly after the release of a relatively brief period of unilateral ureteral obstruction (UUO). However, the long-term impact of hypertension on the recovery of renal functions has not been investigated beyond the immediate period after UUO reversal. In order to investigate this effect, a group of spontaneously hypertensive rats (G-SHR, n = 11) and a group of normotensive Wistar Kyoto rats (G-NTR, n = 11) were subjected to a 48 h reversible left UUO. The impact of UUO was then examined 45 days after the reversal of obstruction. The glomerular filtration rate, renal blood flow, and the fractional excretion of sodium in the post-obstructed left kidney (POK) showed similarities to the non-obstructed right kidney (NOK) in both groups. However, the changes in the albumin creatinine ratio, renal injury markers, pro-apoptotic markers, and histological changes in the G-SHR were much more pronounced compared to the G-NTR. We conclude that hypertension continues to have a significant impact on various aspects of renal injury and function, even several weeks after UUO reversal. Full article
(This article belongs to the Special Issue New Trends in Diabetes, Hypertension and Cardiovascular Diseases 2.0)
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13 pages, 2297 KiB  
Article
Heart Failure Promotes Cancer Progression in an Integrin β1-Dependent Manner
Int. J. Mol. Sci. 2023, 24(24), 17367; https://doi.org/10.3390/ijms242417367 - 11 Dec 2023
Viewed by 835
Abstract
Heart failure and cancer are currently the deadliest diseases in the Western world, posing the most pressing clinical challenges that remain unmet today. Both conditions share similar risk factors, including age, genetics, lifestyle, chronic inflammation, stress, and more. Furthermore, medications that are being [...] Read more.
Heart failure and cancer are currently the deadliest diseases in the Western world, posing the most pressing clinical challenges that remain unmet today. Both conditions share similar risk factors, including age, genetics, lifestyle, chronic inflammation, stress, and more. Furthermore, medications that are being used to counteract cancer frequently result in cardiotoxicity and the spontaneous emergence of heart failure. Thus, heart failure and cancer display an intimate connection and share similarities. Recent studies show that cardiac remodeling and heart failure promote cancer progression and metastasis. Using three different mouse models for heart failure revealed that the communication between the remodeled heart and the tumor is facilitated through multiple secreted factors. Among these factors, Periostin was consistently found to be elevated in all models and was shown to be required in vitro. Yet, whether Periostin is necessary for tumor promotion in vivo is unknown. Towards this end, we examined tumor promotion in mice lacking Periostin following transverse aortic constriction (TAC). Despite the loss of Periostin, tumor growth was promoted in the TAC-operated mice. This likely occurred due to increased levels of various cytokines and growth factors in Periostin KO mice. Many of these factors are potential ligands of Integrin receptors. Therefore, we next studied the role of Integrin receptors in the tumor-promotion phenotype following heart failure. We generated cancer cells with an Integrin β1 loss of function mutation and examined tumor growth in the presence and absence of heart failure. Integrin β1 KO cancer cells fail to display cardiac-remodeling-dependent tumor-promotion. Interestingly, a previous study showed that renal cell carcinoma cells (Renca) fail to be promoted following a myocardial infarction. Consistently, we show that Renca cells do not respond to secreted factors derived from the failing heart both in vitro and in vivo. Interestingly, Renca cells display low basal mRNA levels of Integrin β1 which may explain the inability of heart failure to promote their growth. The findings may have significant clinical relevance to cardio–oncology patients who suffer from cancers with high levels of Integrin β1. Chemotherapy leading to cardiotoxicity in these patients may generate a vicious cycle with poor prognosis. Full article
(This article belongs to the Special Issue New Trends in Diabetes, Hypertension and Cardiovascular Diseases 2.0)
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Review

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21 pages, 1263 KiB  
Review
Novel Diagnostic Methods for Infective Endocarditis
Int. J. Mol. Sci. 2024, 25(2), 1245; https://doi.org/10.3390/ijms25021245 - 19 Jan 2024
Viewed by 892
Abstract
Infective endocarditis (IE) remains a dangerous disease and continues to have a high mortality rate. Unfortunately, despite continuous improvements in diagnostic methods, in many cases, blood cultures remain negative, and the pathogen causing endocarditis is unknown. This makes targeted therapy and the selection [...] Read more.
Infective endocarditis (IE) remains a dangerous disease and continues to have a high mortality rate. Unfortunately, despite continuous improvements in diagnostic methods, in many cases, blood cultures remain negative, and the pathogen causing endocarditis is unknown. This makes targeted therapy and the selection of appropriate antibiotics impossible. Therefore, we present what methods can be used to identify the pathogen in infective endocarditis. These are mainly molecular methods, including PCR and MGS, as well as imaging methods using radiotracers, which offer more possibilities for diagnosing IE. However, they are still not widely used in the diagnosis of IE. The article summarizes in which cases we should choose them and what we are most hopeful about in further research into the diagnosis of IE. In addition, registered clinical trials that are currently underway for the diagnosis of IE are also presented. Full article
(This article belongs to the Special Issue New Trends in Diabetes, Hypertension and Cardiovascular Diseases 2.0)
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27 pages, 4566 KiB  
Review
Animal Models, Pathogenesis, and Potential Treatment of Thoracic Aortic Aneurysm
Int. J. Mol. Sci. 2024, 25(2), 901; https://doi.org/10.3390/ijms25020901 - 11 Jan 2024
Viewed by 800
Abstract
Thoracic aortic aneurysm (TAA) has a prevalence of 0.16–0.34% and an incidence of 7.6 per 100,000 person-years, accounting for 1–2% of all deaths in Western countries. Currently, no effective pharmacological therapies have been identified to slow TAA development and prevent TAA rupture. Large [...] Read more.
Thoracic aortic aneurysm (TAA) has a prevalence of 0.16–0.34% and an incidence of 7.6 per 100,000 person-years, accounting for 1–2% of all deaths in Western countries. Currently, no effective pharmacological therapies have been identified to slow TAA development and prevent TAA rupture. Large TAAs are treated with open surgical repair and less invasive thoracic endovascular aortic repair, both of which have high perioperative mortality risk. Therefore, there is an urgent medical need to identify the cellular and molecular mechanisms underlying TAA development and rupture to develop new therapies. In this review, we summarize animal TAA models including recent developments in porcine and zebrafish models: porcine models can assess new therapeutic devices or intervention strategies in a large mammal and zebrafish models can employ large-scale small-molecule suppressor screening in microwells. The second part of the review covers current views of TAA pathogenesis, derived from recent studies using these animal models, with a focus on the roles of the transforming growth factor-beta (TGFβ) pathway and the vascular smooth muscle cell (VSMC)-elastin-contractile unit. The last part discusses TAA treatment options as they emerge from recent preclinical studies. Full article
(This article belongs to the Special Issue New Trends in Diabetes, Hypertension and Cardiovascular Diseases 2.0)
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