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New Trends in Diabetes, Hypertension and Cardiovascular Diseases 2.0

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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: closed (30 May 2024) | Viewed by 18142

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Special Issue Editors

Dr. Yutang Wang

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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

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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".

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 (10 papers)

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Research

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14 pages, 4335 KiB

Open AccessArticle

Exercise Reduces Glucose Intolerance, Cardiac Inflammation and Adipose Tissue Dysfunction in Psammomys obesus Exposed to Short Photoperiod and High Energy Diet

by Joanne T. M. Tan, Kiara J. Price, Sarah-Rose Fanshaw, Carmel Bilu, Quang Tuan Pham, Anthony Pham, Lauren Sandeman, Victoria A. Nankivell, Emma L. Solly, Noga Kronfeld-Schor and Christina A. Bursill

Int. J. Mol. Sci. 2024, 25(14), 7756; https://doi.org/10.3390/ijms25147756 - 15 Jul 2024

Viewed by 766

Abstract

Circadian disruption causes glucose intolerance, cardiac fibrosis, and adipocyte dysfunction in sand rats (Psammomys obesus). Exercise intervention can improve glucose metabolism, insulin sensitivity, adipose tissue function and protect against inflammation. We investigated the influence of exercise on male P. obesus exposed to a short photoperiod (5 h light:19 h dark) and high-energy diet. Exercise reduced glucose intolerance. Exercise reduced cardiac expression of inflammatory marker Ccl2 and Bax:Bcl2 apoptosis ratio. Exercise increased heart:body weight ratio and hypertrophy marker Myh7:Myh6, yet reduced Gata4 expression. No phenotypic changes were observed in perivascular fibrosis and myocyte area. Exercise reduced visceral adipose expression of inflammatory transcription factor Rela, adipogenesis marker Ppard and browning marker Ppargc1a, but visceral adipocyte size was unaffected. Conversely, exercise reduced subcutaneous adipocyte size but did not affect any molecular mediators. Exercise increased ZT7 Bmal1 and Per2 in the suprachiasmatic nucleus and subcutaneous Per2. Our study provides new molecular insights and histological assessments on the effect of exercise on cardiac inflammation, adipose tissue dysfunction and circadian gene expression in P. obesus exposed to short photoperiod and high-energy diet. These findings have implications for the protective benefits of exercise for shift workers in order to reduce the risk of diabetes and cardiovascular disease. Full article

(This article belongs to the Special Issue New Trends in Diabetes, Hypertension and Cardiovascular Diseases 2.0)

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19 pages, 4387 KiB

Open AccessArticle

Female Psammomys obesus Are Protected from Circadian Disruption-Induced Glucose Intolerance, Cardiac Fibrosis and Adipocyte Dysfunction

by Joanne T. M. Tan, Cate V. Cheney, Nicole E. S. Bamhare, Tasnim Hossin, Carmel Bilu, Lauren Sandeman, Victoria A. Nankivell, Emma L. Solly, Noga Kronfeld-Schor and Christina A. Bursill

Int. J. Mol. Sci. 2024, 25(13), 7265; https://doi.org/10.3390/ijms25137265 - 1 Jul 2024

Viewed by 763

Abstract

Circadian disruption increases the development of cardiovascular disease and diabetes. We found that circadian disruption causes glucose intolerance, cardiac fibrosis and adipocyte tissue dysfunction in male sand rats, Psammomys obesus. Whether these effects occur in female P. obesus is unknown. Male and female P. obesus were fed a high energy diet and exposed to a neutral (12 light:12 dark, control) or short (5 light:19 dark, circadian disruption) photoperiod for 20 weeks. Circadian disruption impaired glucose tolerance in males but not females. It also increased cardiac perivascular fibrosis and cardiac expression of inflammatory marker Ccl2 in males, with no effect in females. Females had reduced proapoptotic Bax mRNA and cardiac Myh7:Myh6 hypertrophy ratio. Cardiac protection in females occurred despite reductions in the clock gene Per2. Circadian disruption increased adipocyte hypertrophy in both males and females. This was concomitant with a reduction in adipocyte differentiation markers Pparg and Cebpa in males and females, respectively. Circadian disruption increased visceral adipose expression of inflammatory mediators Ccl2, Tgfb1 and Cd68 and reduced browning marker Ucp1 in males. However, these changes were not observed in females. Collectively, our study show that sex differentially influences the effects of circadian disruption on glucose tolerance, cardiac function and adipose tissue dysfunction. Full article

(This article belongs to the Special Issue New Trends in Diabetes, Hypertension and Cardiovascular Diseases 2.0)

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43 pages, 8752 KiB

Open AccessArticle

T-Cell Receptor Sequences Identify Combined Coxsackievirus–Streptococci Infections as Triggers for Autoimmune Myocarditis and Coxsackievirus–Clostridia Infections for Type 1 Diabetes

by Robert Root-Bernstein

Int. J. Mol. Sci. 2024, 25(3), 1797; https://doi.org/10.3390/ijms25031797 - 1 Feb 2024

Viewed by 1737

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 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

Open AccessArticle

Does Hypertension Affect the Recovery of Renal Functions after Reversal of Unilateral Ureteric Obstruction?

by Fayez T. Hammad, Loay Lubbad, Suhail Al-Salam, Waheed F. Hammad, Javed Yasin, Mohamed Fizur Nagoor Meeran, Shreesh Ojha, Seenipandi Arunachalam and Awwab F. Hammad

Int. J. Mol. Sci. 2024, 25(3), 1540; https://doi.org/10.3390/ijms25031540 - 26 Jan 2024

Viewed by 719

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 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

Open AccessArticle

Heart Failure Promotes Cancer Progression in an Integrin β1-Dependent Manner

by Irina Langier Goncalves, Lama Awwad, Sharon Aviram, Talel Izraeli, Laris Achlaug and Ami Aronheim

Int. J. Mol. Sci. 2023, 24(24), 17367; https://doi.org/10.3390/ijms242417367 - 11 Dec 2023

Cited by 1 | Viewed by 1299

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 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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87 pages, 3719 KiB

Open AccessReview

Beyond Anticoagulation: A Comprehensive Review of Non-Vitamin K Oral Anticoagulants (NOACs) in Inflammation and Protease-Activated Receptor Signaling

by Shirin Jannati, Rajashree Patnaik and Yajnavalka Banerjee

Int. J. Mol. Sci. 2024, 25(16), 8727; https://doi.org/10.3390/ijms25168727 - 10 Aug 2024

Viewed by 355

Abstract

Non-vitamin K oral anticoagulants (NOACs) have revolutionized anticoagulant therapy, offering improved safety and efficacy over traditional agents like warfarin. This review comprehensively examines the dual roles of NOACs—apixaban, rivaroxaban, edoxaban, and dabigatran—not only as anticoagulants, but also as modulators of inflammation via protease-activated receptor (PAR) signaling. We highlight the unique pharmacotherapeutic properties of each NOAC, supported by key clinical trials demonstrating their effectiveness in preventing thromboembolic events. Beyond their established anticoagulant roles, emerging research suggests that NOACs influence inflammation through PAR signaling pathways, implicating factors such as factor Xa (FXa) and thrombin in the modulation of inflammatory responses. This review synthesizes current evidence on the anti-inflammatory potential of NOACs, exploring their impact on inflammatory markers and conditions like atherosclerosis and diabetes. By delineating the mechanisms by which NOACs mediate anti-inflammatory effects, this work aims to expand their therapeutic utility, offering new perspectives for managing inflammatory diseases. Our findings underscore the broader clinical implications of NOACs, advocating for their consideration in therapeutic strategies aimed at addressing inflammation-related pathologies. This comprehensive synthesis not only enhances understanding of NOACs’ multifaceted roles, but also paves the way for future research and clinical applications in inflammation and cardiovascular health. Full article

(This article belongs to the Special Issue New Trends in Diabetes, Hypertension and Cardiovascular Diseases 2.0)

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16 pages, 994 KiB

Open AccessReview

Epigenetic Regulation of the Renin–Angiotensin–Aldosterone System in Hypertension

by Yoshimichi Takeda, Masashi Demura, Takashi Yoneda and Yoshiyu Takeda

Int. J. Mol. Sci. 2024, 25(15), 8099; https://doi.org/10.3390/ijms25158099 - 25 Jul 2024

Viewed by 457

Abstract

Activation of the renin–angiotensin–aldosterone system (RAAS) plays an important pathophysiological role in hypertension. Increased mRNA levels of the angiotensinogen angiotensin-converting enzyme, angiotensin type 1 receptor gene, Agtr1a, and the aldosterone synthase gene, CYP11B2, have been reported in the heart, blood vessels, and kidneys in salt-sensitive hypertension. However, the mechanism of gene regulation in each component of the RAAS in cardiovascular and renal tissues is unclear. Epigenetic mechanisms, which are important for regulating gene expression, include DNA methylation, histone post-translational modifications, and microRNA (miRNA) regulation. A close association exists between low DNA methylation at CEBP-binding sites and increased AGT expression in visceral adipose tissue and the heart of salt-sensitive hypertensive rats. Several miRNAs influence AGT expression and are associated with cardiovascular diseases. Expression of both ACE and ACE2 genes is regulated by DNA methylation, histone modifications, and miRNAs. Expression of both angiotensinogen and CYP11B2 is reversibly regulated by epigenetic modifications and is related to salt-sensitive hypertension. The mineralocorticoid receptor (MR) exists in cardiovascular and renal tissues, in which many miRNAs influence expression and contribute to the pathogenesis of hypertension. Expression of the 11beta-hydroxysteroid dehydrogenase type 2 (HSD11B2) gene is also regulated by methylation and miRNAs. Epigenetic regulation of renal and vascular HSD11B2 is an important pathogenetic mechanism for salt-sensitive hypertension. Full article

(This article belongs to the Special Issue New Trends in Diabetes, Hypertension and Cardiovascular Diseases 2.0)

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36 pages, 1220 KiB

Open AccessReview

Immunomodulation through Nutrition Should Be a Key Trend in Type 2 Diabetes Treatment

by Katarzyna Napiórkowska-Baran, Paweł Treichel, Marta Czarnowska, Magdalena Drozd, Kinga Koperska, Agata Węglarz, Oskar Schmidt, Samira Darwish, Bartłomiej Szymczak and Zbigniew Bartuzi

Int. J. Mol. Sci. 2024, 25(7), 3769; https://doi.org/10.3390/ijms25073769 - 28 Mar 2024

Viewed by 1169

Abstract

An organism’s ability to function properly depends not solely on its diet but also on the intake of nutrients and non-nutritive bioactive compounds that exert immunomodulatory effects. This principle applies both to healthy individuals and, in particular, to those with concomitant chronic conditions, such as type 2 diabetes. However, the current food industry and the widespread use of highly processed foods often lead to nutritional deficiencies. Numerous studies have confirmed the occurrence of immune system dysfunction in patients with type 2 diabetes. This article elucidates the impact of specific nutrients on the immune system function, which maintains homeostasis of the organism, with a particular emphasis on type 2 diabetes. The role of macronutrients, micronutrients, vitamins, and selected substances, such as omega-3 fatty acids, coenzyme Q10, and alpha-lipoic acid, was taken into consideration, which outlined the minimum range of tests that ought to be performed on patients in order to either directly or indirectly determine the severity of malnutrition in this group of patients. Full article

(This article belongs to the Special Issue New Trends in Diabetes, Hypertension and Cardiovascular Diseases 2.0)

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21 pages, 1263 KiB

Open AccessReview

Novel Diagnostic Methods for Infective Endocarditis

by Anna Burban, Dorota Słupik, Aleksandra Reda, Ewa Szczerba, Marcin Grabowski and Agnieszka Kołodzińska

Int. J. Mol. Sci. 2024, 25(2), 1245; https://doi.org/10.3390/ijms25021245 - 19 Jan 2024

Cited by 2 | Viewed by 2582

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 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

Open AccessReview

Animal Models, Pathogenesis, and Potential Treatment of Thoracic Aortic Aneurysm

by Yutang Wang, Indu S. Panicker, Jack Anesi, Owen Sargisson, Benjamin Atchison and Andreas J. R. Habenicht

Int. J. Mol. Sci. 2024, 25(2), 901; https://doi.org/10.3390/ijms25020901 - 11 Jan 2024

Cited by 1 | Viewed by 2082

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 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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