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Biomolecules
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Heart Failure: Molecular Mechanisms and Novel Therapeutic Approaches
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Heart Failure: Molecular Mechanisms and Novel Therapeutic Approaches

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

Deadline for manuscript submissions: closed (15 March 2022) | Viewed by 14618

Special Issue Editor

Prof. Dr. Blanche Schroen

E-Mail Website
Guest Editor
Department of Physiology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands
Interests: non-coding RNA; (diastolic) heart failure; inflammation; cellular metabolism; microvascular function; fibrosis; sex differences

Special Issue Information

Dear Colleagues,

This Special Issue is about current knowledge of and insights into the role of non-coding RNAs in the pathophysiology of heart failure. Heart failure, in particular with a preserved ejection fraction (HFpEF), is the result of a complex interplay between the heart and systemic (metabolic) derangements. In the heart, (coronary) (micro)vasculature, connective tissue structure, electric management, inflammatory milieu and cardiomyocyte functions are all affected. In the circulation supplying the heart, systemic (metabolic) derangements associated with heart failure risk factors, such as diabetes, obesity and hypertension, lead to changes in metabolites, nutrients, (endothelial) cell-shed content and platelet and immune cell functions. Moreover, sex differences seem to play a role in heart failure susceptibility, among which hormonal influences have been the subject of investigations.

Non-coding RNAs are now established as therapeutic targets. Still, there is no cure for heart failure. Here, we welcome papers that contribute to a clarification of current knowledge of and insights into the role of non-coding RNAs in the complex playing field characterizing failing heart.

Prof. Blanche Schroen
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

  • non-coding RNA
  • cardiac (diastolic) dysfunction
  • microvascular dysfunction
  • inflammation
  • fibrosis
  • cardiomyocyte metabolism
  • cardiomyocyte stiffness
  • atrial fibrillation
  • sex differences
  • metabolic disease
  • platelet function in cardiac pathology

Published Papers (4 papers)

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Research

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15 pages, 2709 KiB  
Article
Cardioprotective Effect of Glycyrrhizin on Myocardial Remodeling in Diabetic Rats
by Vikram Thakur, Narah Alcoreza, Monica Delgado, Binata Joddar and Munmun Chattopadhyay
Biomolecules 2021, 11(4), 569; https://doi.org/10.3390/biom11040569 - 13 Apr 2021
Cited by 20 | Viewed by 3515
Abstract
Myocardial fibrosis is one of the major complications of long-term diabetes. Hyperglycemia induced cardiomyocyte atrophy is a frequent pathophysiological indicator of diabetic heart. The objective of this study was to investigate the cardioprotective effect of glycyrrhizin (GLC) on myocardial damage in diabetic rats [...] Read more.
Myocardial fibrosis is one of the major complications of long-term diabetes. Hyperglycemia induced cardiomyocyte atrophy is a frequent pathophysiological indicator of diabetic heart. The objective of this study was to investigate the cardioprotective effect of glycyrrhizin (GLC) on myocardial damage in diabetic rats and assess the anti-inflammatory and anti-fibrotic effect of GLC. Our study demonstrates that hyperglycemia can elevate cardiac atrophy in diabetic animals. Type 2 diabetic fatty and the lean control rats were evaluated for cardiac damage and inflammation at 8–12 weeks after the development of diabetes. Western blot and immunohistochemical studies revealed that gap junction protein connexin-43 (CX43), cardiac injury marker troponin I, cardiac muscle specific voltage gated sodium channel NaV1.5 were significantly altered in the diabetic heart. Furthermore, oxidative stress mediator receptor for advanced glycation end-products (RAGE), as well as inflammatory mediator phospho-p38 MAPK and chemokine receptor CXCR4 were increased in the diabetic heart whereas the expression of nuclear factor erythroid-2-related factor 2 (Nrf2), the antioxidant proteins that protect against oxidative damage was reduced. We also observed an increase in the expression of the pleiotropic cytokine, transforming growth factor beta (TGF-β) in the diabetic heart. GLC treatment exhibited a decrease in the expression of phospho-p38 MAPK, RAGE, NaV1.5 and TGF-β and it also altered the expression of CX43, CXCR4, Nrf2 and troponin I. These observations suggest that GLC possesses cardioprotective effects in diabetic cardiac atrophy and that these effects could be mediated through activation of Nrf2 and inhibition of CXCR4/SDF1 as well as TGF-β/p38MAPK signaling pathway. Full article
(This article belongs to the Special Issue Heart Failure: Molecular Mechanisms and Novel Therapeutic Approaches)
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Review

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21 pages, 3886 KiB  
Review
Noninvasive Cardiac Imaging in Formerly Preeclamptic Women for Early Detection of Subclinical Myocardial Abnormalities: A 2022 Update
by Yentl Brandt, Chahinda Ghossein-Doha, Suzanne C. Gerretsen, Marc E. A. Spaanderman and M. Eline Kooi
Biomolecules 2022, 12(3), 415; https://doi.org/10.3390/biom12030415 - 7 Mar 2022
Cited by 2 | Viewed by 2715
Abstract
Preeclampsia is a maternal hypertensive disease, complicating 2–8% of all pregnancies. It has been linked to a 2–7-fold increased risk for the development of cardiovascular disease, including heart failure, later in life. A total of 40% of formerly preeclamptic women develop preclinical heart [...] Read more.
Preeclampsia is a maternal hypertensive disease, complicating 2–8% of all pregnancies. It has been linked to a 2–7-fold increased risk for the development of cardiovascular disease, including heart failure, later in life. A total of 40% of formerly preeclamptic women develop preclinical heart failure, which may further deteriorate into clinical heart failure. Noninvasive cardiac imaging could assist in the early detection of myocardial abnormalities, especially in the preclinical stage, when these changes are likely to be reversible. Moreover, imaging studies can improve our insights into the relationship between preeclampsia and heart failure and can be used for monitoring. Cardiac ultrasound is used to assess quantitative changes, including the left ventricular cavity volume and wall thickness, myocardial mass, systolic and diastolic function, and strain. Cardiac magnetic resonance imaging may be of additional diagnostic value to assess diffuse and focal fibrosis and perfusion. After preeclampsia, sustained elevated myocardial mass along with reduced myocardial circumferential and longitudinal strain and decreased diastolic function is reported. These findings are consistent with the early phases of heart failure, referred to as preclinical (asymptomatic) or B-stage heart failure. In this review, we will provide an up-to-date overview of the potential of cardiac magnetic resonance imaging and echocardiography in identifying formerly preeclamptic women who are at high risk for developing heart failure. The potential contribution to early cardiac screening of women with a history of preeclampsia and the pros and cons of these imaging modalities are outlined. Finally, recommendations for future research are presented. Full article
(This article belongs to the Special Issue Heart Failure: Molecular Mechanisms and Novel Therapeutic Approaches)
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29 pages, 1558 KiB  
Review
The Role of Systemic Microvascular Dysfunction in Heart Failure with Preserved Ejection Fraction
by Jerremy Weerts, Sanne G. J. Mourmans, Arantxa Barandiarán Aizpurua, Blanche L. M. Schroen, Christian Knackstedt, Etto Eringa, Alfons J. H. M. Houben and Vanessa P. M. van Empel
Biomolecules 2022, 12(2), 278; https://doi.org/10.3390/biom12020278 - 9 Feb 2022
Cited by 12 | Viewed by 5402
Abstract
Heart failure with preserved ejection fraction (HFpEF) is a condition with increasing incidence, leading to a health care problem of epidemic proportions for which no curative treatments exist. Consequently, an urge exists to better understand the pathophysiology of HFpEF. Accumulating evidence suggests a [...] Read more.
Heart failure with preserved ejection fraction (HFpEF) is a condition with increasing incidence, leading to a health care problem of epidemic proportions for which no curative treatments exist. Consequently, an urge exists to better understand the pathophysiology of HFpEF. Accumulating evidence suggests a key pathophysiological role for coronary microvascular dysfunction (MVD), with an underlying mechanism of low-grade pro-inflammatory state caused by systemic comorbidities. The systemic entity of comorbidities and inflammation in HFpEF imply that patients develop HFpEF due to systemic mechanisms causing coronary MVD, or systemic MVD. The absence or presence of peripheral MVD in HFpEF would reflect HFpEF being predominantly a cardiac or a systemic disease. Here, we will review the current state of the art of cardiac and systemic microvascular dysfunction in HFpEF (Graphical Abstract), resulting in future perspectives on new diagnostic modalities and therapeutic strategies. Full article
(This article belongs to the Special Issue Heart Failure: Molecular Mechanisms and Novel Therapeutic Approaches)
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Graphical abstract

14 pages, 953 KiB  
Review
Changes in Cardiac Metabolism in Prediabetes
by Vera H. W. de Wit-Verheggen and Tineke van de Weijer
Biomolecules 2021, 11(11), 1680; https://doi.org/10.3390/biom11111680 - 12 Nov 2021
Cited by 5 | Viewed by 2030
Abstract
In type 2 diabetes mellitus (T2DM), there is an increased prevalence of cardiovascular disease (CVD), even when corrected for atherosclerosis and other CVD risk factors. Diastolic dysfunction is one of the early changes in cardiac function that precedes the onset of cardiac failure, [...] Read more.
In type 2 diabetes mellitus (T2DM), there is an increased prevalence of cardiovascular disease (CVD), even when corrected for atherosclerosis and other CVD risk factors. Diastolic dysfunction is one of the early changes in cardiac function that precedes the onset of cardiac failure, and it occurs already in the prediabetic state. It is clear that these changes are closely linked to alterations in cardiac metabolism; however, the exact etiology is unknown. In this narrative review, we provide an overview of the early cardiac changes in fatty acid and glucose metabolism in prediabetes and its consequences on cardiac function. A better understanding of the relationship between metabolism, mitochondrial function, and cardiac function will lead to insights into the etiology of the declined cardiac function in prediabetes. Full article
(This article belongs to the Special Issue Heart Failure: Molecular Mechanisms and Novel Therapeutic Approaches)
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