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Biomolecules
Special Issues
Heart Diseases: Molecular Mechanisms and New Therapies
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Heart Diseases: Molecular Mechanisms and New Therapies

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

Deadline for manuscript submissions: closed (30 April 2025) | Viewed by 9107

Special Issue Editor

Dr. Glen Pyle

E-Mail Website
Guest Editor
1. IMPART Network, Dalhousie Medicine, 100 Tucker Park Rd., Saint John, NB E2K 5E2, Canada
2. Women’s Health Research Institute, BC Women’s Hospital + Health Centre, H214 – 4500 Oak Street, Box 42B, Vancouver, BC V6H 3N1, Canada
3. Department of Biomedical Sciences, Ontario Veterinary College, University of Guelph, Guelph, ON, Canada
Interests: molecular basis of heart failure; molecular therapeutics; sex differences in cardiovascular health and disease; menopause
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to invite you to submit original research articles and reviews on the molecular mechanisms and novel therapies for heart diseases. Cardiovascular disease is a leading cause of death globally and its incidence is growing. Understanding the molecular changes that occur in the heart during the development of disease is critical to creating and applying novel therapies to treat heart diseases.

This Special Issue aims to highlight and promote our understanding of heart disease, including its molecular basis and emerging therapies to treat these conditions. Papers focused on a range of cardiac conditions, from genetic cardiomyopathies to ischemia-reperfusion injury, and stressors that impact heart function, from diabetes and hypertension to pregnancy and menopause, are welcomed. Furthermore, we invite studies that are fundamental in nature and use animal models of disease, alongside research involving patients and their care. The focus of studies and reviews should be identifying the molecular mechanisms of conditions that impact the heart and/or testing novel therapeutic strategies that mitigate dysfunction and injury.

I/We look forward to receiving your contributions.

Dr. Glen Pyle
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. 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

  • heart failure
  • heart disease
  • myocardial
  • molecular mechanisms
  • therapies

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Published Papers (5 papers)

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Research

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16 pages, 13174 KiB  
Article
MicroRNA-150 Deletion from Adult Myofibroblasts Augments Maladaptive Cardiac Remodeling Following Chronic Myocardial Infarction
by Satoshi Kawaguchi, Marisa N. Sepúlveda, Jian-peng Teoh, Taiki Hayasaka, Bruno Moukette, Tatsuya Aonuma, Hyun Cheol Roh, Meena S. Madhur and Il-man Kim
Biomolecules 2024, 14(12), 1650; https://doi.org/10.3390/biom14121650 - 22 Dec 2024
Viewed by 1080
Abstract
MicroRNA (miR: small noncoding RNA)-150 is evolutionarily conserved and is downregulated in patients with diverse forms of heart failure (HF) and in multiple mouse models of HF. Moreover, miR-150 is markedly correlated with the outcome of patients with HF. We previously reported that [...] Read more.
MicroRNA (miR: small noncoding RNA)-150 is evolutionarily conserved and is downregulated in patients with diverse forms of heart failure (HF) and in multiple mouse models of HF. Moreover, miR-150 is markedly correlated with the outcome of patients with HF. We previously reported that systemic or cardiomyocyte-derived miR-150 in mice elicited myocardial protection through the inhibition of cardiomyocyte death, without affecting neovascularization and T cell infiltration. Our mechanistic studies also showed that the protective roles of miR-150 in ischemic mouse hearts and human cardiac fibroblasts were, in part, attributed to the inhibition of fibroblast activation via the repression of multiple profibrotic genes. However, the extent to which miR-150 expression in adult myofibroblasts (MFs) modulates the response to myocardial infarction (MI) remains unknown. Here, we develop a novel 4-hydroxytamoxifen-inducible MF-specific miR-150 conditional knockout mouse model and demonstrate that the mouse line exhibits worse cardiac dysfunction after MI. Our studies further reveal that miR-150 ablation selectively in adult MFs exacerbates cardiac damage and apoptosis after chronic MI. Lastly, MF-specific miR-150 deletion in adult mice promotes the expression of proinflammatory and profibrotic genes as well as cardiac fibrosis following chronic MI. Our findings indicate a key protective role for MF-derived miR-150 in modulating post-MI responses. Full article
(This article belongs to the Special Issue Heart Diseases: Molecular Mechanisms and New Therapies)
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21 pages, 4000 KiB  
Article
Yap Is a Nutrient Sensor Sensitive to the Amino Acid L-Isoleucine and Regulates the Expression of Ctgf in Cardiomyocytes
by Victoria L. Nelson, Ashley L. Eadie, Lester Perez, Malav Madhu, Mathew Platt, Angella Mercer, Thomas Pulinilkunnil, Petra Kienesberger, Jeremy A. Simpson and Keith R. Brunt
Biomolecules 2024, 14(10), 1299; https://doi.org/10.3390/biom14101299 - 14 Oct 2024
Cited by 2 | Viewed by 1791
Abstract
Myocardial infarction and reperfusion constitute a complex injury consisting of many distinct molecular stress patterns that influence cardiomyocyte survival and adaptation. Cell signalling, which is essential to cardiac development, also presents potential disease-modifying opportunities to recover and limit myocardial injury or maladaptive remodelling. [...] Read more.
Myocardial infarction and reperfusion constitute a complex injury consisting of many distinct molecular stress patterns that influence cardiomyocyte survival and adaptation. Cell signalling, which is essential to cardiac development, also presents potential disease-modifying opportunities to recover and limit myocardial injury or maladaptive remodelling. Here, we hypothesized that Yap signalling could be sensitive to one or more molecular stress patterns associated with early acute ischemia. We found that Yap, and not Taz, expression patterns differed in a post-myocardial infarct compared to a peri-infarct region of rat hearts post-myocardial infarction, suggesting cell specificity that would be challenging to resolve for causation in vivo. Using H9c2 ventricular myotubes in vitro as a model, Yap levels were determined to be more sensitive to nutrient deprivation than other stress patterns typified by ischemia within the first hour of stress. Moreover, this is mediated by amino acid availability, predominantly L-isoleucine, and influences the expression of connective tissue growth factor (Ctgf)—a major determinant of myocardial adaptation after injury. These findings present novel opportunities for future therapeutic development and risk assessment for myocardial injury and adaptation. Full article
(This article belongs to the Special Issue Heart Diseases: Molecular Mechanisms and New Therapies)
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15 pages, 1446 KiB  
Article
Perimenopause Decreases SERCA2a Activity in the Hearts of a Mouse Model of Ovarian Failure
by Ciara Barry, Sarah Rouhana, Jessica L. Braun, Mia S. Geromella, Val A. Fajardo and W. Glen Pyle
Biomolecules 2024, 14(6), 675; https://doi.org/10.3390/biom14060675 - 9 Jun 2024
Cited by 3 | Viewed by 2145
Abstract
Risk of cardiovascular disease mortality rises in women after menopause. While increased cardiovascular risk is largely attributed to postmenopausal declines in estrogens, the molecular changes in the heart that contribute to risk are poorly understood. Disruptions in intracellular calcium handling develop in ovariectomized [...] Read more.
Risk of cardiovascular disease mortality rises in women after menopause. While increased cardiovascular risk is largely attributed to postmenopausal declines in estrogens, the molecular changes in the heart that contribute to risk are poorly understood. Disruptions in intracellular calcium handling develop in ovariectomized mice and have been implicated in cardiac dysfunction. Using a mouse model of menopause in which ovarian failure occurs over 120 days, we sought to determine if perimenopause impacted calcium removal mechanisms in the heart and identify the molecular mechanisms. Mice were injected with 4-vinylcyclohexene diepoxide (VCD) to induce ovarian failure over 120 days, mimicking perimenopause. Hearts were removed at 60 and 120 days after VCD injections, representing the middle and end of perimenopause. SERCA2a function was significantly diminished at the end of perimenopause. Neither SERCA2a nor phospholamban expression changed at either time point, but phospholamban phosphorylation at S16 and T17 was dynamically altered. Intrinsic SERCA inhibitors sarcolipin and myoregulin increased >4-fold at day 60, as did the native activator DWORF. At the end of perimenopause, sarcolipin and myoregulin returned to baseline levels while DWORF was significantly reduced below controls. Sodium–calcium exchanger expression was significantly increased at the end of perimenopause. These results show that the foundation for increased cardiovascular disease mortality develops in the heart during perimenopause and that regulators of calcium handling exhibit significant fluctuations over time. Understanding the temporal development of cardiovascular risk associated with menopause and the underlying mechanisms is critical to developing interventions that mitigate the rise in cardiovascular mortality that arises after menopause. Full article
(This article belongs to the Special Issue Heart Diseases: Molecular Mechanisms and New Therapies)
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Review

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14 pages, 1310 KiB  
Review
Sex-Specific Differences in the Pathophysiology of Hypertension
by Hannah Zhang, Pawan K. Singal, Amir Ravandi and Inna Rabinovich-Nikitin
Biomolecules 2025, 15(1), 143; https://doi.org/10.3390/biom15010143 - 18 Jan 2025
Cited by 1 | Viewed by 1947
Abstract
Hypertension is one of the most common comorbidities in cardiometabolic diseases, affecting nearly one third of adults. As a result, its pathophysiological mechanisms have been studied extensively and are focused around pressure natriuresis, the renin–angiotensin system (RAS), the sympathetic nervous system, oxidative stress, [...] Read more.
Hypertension is one of the most common comorbidities in cardiometabolic diseases, affecting nearly one third of adults. As a result, its pathophysiological mechanisms have been studied extensively and are focused around pressure natriuresis, the renin–angiotensin system (RAS), the sympathetic nervous system, oxidative stress, and endothelial dysfunction. Additionally, hypertension secondary to other underlying etiologies also exists. While clinical evidence has clearly shown differences in hypertension development in males and females, relatively little is known about the pathophysiological mechanisms behind these differences. Sex hormones likely play a key role, as they modulate many factors related to hypertension development. In this review, we postulate the potential role for sexually dimorphic fat metabolism in the physiology of hypertension. In brief, estrogen promotes subcutaneous fat deposition over visceral fat and increases in mass via adaptive hyperplasia rather than pathogenic hypertrophy. This adipose tissue subsequently produces anti-inflammatory effects and inhibits metabolic dysfunction-associated fatty liver disease (MAFLD) and RAS activation, ultimately leading to decreased levels of hypertension in pre-menopausal females. On the other hand, androgens and the lack of estrogens promote visceral and ectopic fat deposition, including in the liver, and lead to increased circulating pro-inflammatory cytokines and potentially subsequent RAS activation and hypertension development in males and post-menopausal females. Understanding the sex-specific differences in fat metabolism may provide deeper insights into the patho-mechanisms associated with hypertension and lead to more comprehensive sex-specific care. Full article
(This article belongs to the Special Issue Heart Diseases: Molecular Mechanisms and New Therapies)
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23 pages, 1507 KiB  
Review
Mitochondrial Dysfunction in Cardiac Disease: The Fort Fell
by Ioannis Paraskevaidis, Christos Kourek, Dimitrios Farmakis and Elias Tsougos
Biomolecules 2024, 14(12), 1534; https://doi.org/10.3390/biom14121534 - 29 Nov 2024
Cited by 4 | Viewed by 1319
Abstract
Myocardial cells and the extracellular matrix achieve their functions through the availability of energy. In fact, the mechanical and electrical properties of the heart are heavily dependent on the balance between energy production and consumption. The energy produced is utilized in various forms, [...] Read more.
Myocardial cells and the extracellular matrix achieve their functions through the availability of energy. In fact, the mechanical and electrical properties of the heart are heavily dependent on the balance between energy production and consumption. The energy produced is utilized in various forms, including kinetic, dynamic, and thermal energy. Although total energy remains nearly constant, the contribution of each form changes over time. Thermal energy increases, while dynamic and kinetic energy decrease, ultimately becoming insufficient to adequately support cardiac function. As a result, toxic byproducts, unfolded or misfolded proteins, free radicals, and other harmful substances accumulate within the myocardium. This leads to the failure of crucial processes such as myocardial contraction–relaxation coupling, ion exchange, cell growth, and regulation of apoptosis and necrosis. Consequently, both the micro- and macro-architecture of the heart are altered. Energy production and consumption depend on the heart’s metabolic resources and the functional state of the cardiac structure, including cardiomyocytes, non-cardiomyocyte cells, and their metabolic and energetic behavior. Mitochondria, which are intracellular organelles that produce more than 95% of ATP, play a critical role in fulfilling all these requirements. Therefore, it is essential to gain a deeper understanding of their anatomy, function, and homeostatic properties. Full article
(This article belongs to the Special Issue Heart Diseases: Molecular Mechanisms and New Therapies)
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