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Heart Failure Mechanisms and Treatment Advances
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Heart Failure Mechanisms and Treatment Advances

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 (31 October 2024) | Viewed by 5408

Special Issue Editor

Dr. Rabea Asleh

E-Mail Website
Guest Editor
Hadassah University Medical Center, Hebrew University of Jerusalem, Jerusalem, Israel
Interests: heart failure; cardiomyopathy; microbiome; atherosclerosis and CAD; diabetes and obesity
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Heart failure is a complex growing global health problem with a high mortality rate and significant morbidity. Basic and transitional research in this field has provided valuable insights into the molecular, cellular, and physiological changes that occur in cardiomyopathy and heart failure. However, further research is needed to unravel the intricate mechanisms involved and identify novel therapeutic targets that can improve outcomes for patients with heart failure. This Special Issue seeks to address the underlying mechanisms behind the development and progression of various cardiomyopathies and heart failure, shedding light on novel therapeutic approaches to improve patient outcomes.

This issue, “Heart Failure Mechanisms and Treatment Advances”, calls for original research articles from researchers in the field of cardiology and related disciplines. Contributions may cover a wide range of topics, including but not limited to the pathophysiology of heart failure, cellular and molecular mechanisms involved, genetic and epigenetic factors, biomarkers for early detection and prognosis, novel imaging techniques for assessing cardiac function, and emerging treatment strategies. We encourage you to share your expertise and contribute original articles that advance our knowledge of heart failure mechanisms and highlight the latest advances in treatment options.

Dr. Rabea Asleh
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. 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

  • heart failure
  • cardiomyopathy
  • mechanisms
  • inflammation
  • oxidative stress
  • genetic susceptibility
  • microbiome
  • neurohormonal regulation
  • obesity and metabolic syndrome
  • targeted therapies

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Published Papers (3 papers)

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Research

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16 pages, 6502 KiB  
Article
Expression of Osteopontin and Gremlin 1 Proteins in Cardiomyocytes in Ischemic Heart Failure
by Milda Kuprytė, Vaiva Lesauskaitė, Vitalija Siratavičiūtė, Lina Utkienė, Lina Jusienė and Dalia Pangonytė
Int. J. Mol. Sci. 2024, 25(15), 8240; https://doi.org/10.3390/ijms25158240 - 28 Jul 2024
Viewed by 721
Abstract
A relevant role of osteopontin (OPN) and gremlin 1 (Grem1) in regulating cardiac tissue remodeling and formation of heart failure (HF) are documented, with the changes of OPN and Grem1 levels in blood plasma due to acute ischemia, ischemic heart disease-induced advanced HF [...] Read more.
A relevant role of osteopontin (OPN) and gremlin 1 (Grem1) in regulating cardiac tissue remodeling and formation of heart failure (HF) are documented, with the changes of OPN and Grem1 levels in blood plasma due to acute ischemia, ischemic heart disease-induced advanced HF or dilatative cardiomyopathy being the primary focus in most of these studies. However, knowledge on the early OPN and Grem1 proteins expression changes within cardiomyocytes during remodeling due to chronic ischemia remains insufficient. The aim of this study was to determine the OPN and Grem1 proteins expression changes in human cardiomyocytes at different stages of ischemic HF. A semi-quantitative immunohistochemical analysis was performed in 105 myocardial tissue samples obtained from the left cardiac ventricles. Increased OPN immunostaining intensity was already detected in the stage A HF group, compared to the control group (p < 0.001), and continued to increase in the stage B HF (p < 0.001), achieving the peak of immunostaining in the stages C/D HF group (p < 0.001). Similar data of Grem1 immunostaining intensity changes in cardiomyocytes were documented. Significantly positive correlations were detected between OPN, Grem1 expression in cardiomyocytes and their diameter as well as the length, in addition to positive correlation between OPN and Grem1 expression changes within cardiomyocytes. These novel findings suggest that OPN and Grem1 contribute significantly to reorganization of cellular geometry from the earliest stage of cardiomyocyte remodeling, providing new insights into the ischemic HF pathogenesis. Full article
(This article belongs to the Special Issue Heart Failure Mechanisms and Treatment Advances)
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20 pages, 4584 KiB  
Article
Liraglutide Pretreatment Does Not Improve Acute Doxorubicin-Induced Cardiotoxicity in Rats
by Carolina R. Tonon, Marina G. Monte, Paola S. Balin, Anderson S. S. Fujimori, Ana Paula D. Ribeiro, Natália F. Ferreira, Nayane M. Vieira, Ronny P. Cabral, Marina P. Okoshi, Katashi Okoshi, Leonardo A. M. Zornoff, Marcos F. Minicucci, Sergio A. R. Paiva, Mariana J. Gomes and Bertha F. Polegato
Int. J. Mol. Sci. 2024, 25(11), 5833; https://doi.org/10.3390/ijms25115833 - 27 May 2024
Viewed by 1063
Abstract
Doxorubicin is an effective drug for cancer treatment; however, cardiotoxicity limits its use. Cardiotoxicity pathophysiology is multifactorial. GLP-1 analogues have been shown to reduce oxidative stress and inflammation. In this study, we evaluated the effect of pretreatment with liraglutide on doxorubicin-induced acute cardiotoxicity. [...] Read more.
Doxorubicin is an effective drug for cancer treatment; however, cardiotoxicity limits its use. Cardiotoxicity pathophysiology is multifactorial. GLP-1 analogues have been shown to reduce oxidative stress and inflammation. In this study, we evaluated the effect of pretreatment with liraglutide on doxorubicin-induced acute cardiotoxicity. A total of 60 male Wistar rats were allocated into four groups: Control (C), Doxorubicin (D), Liraglutide (L), and Doxorubicin + Liraglutide (DL). L and DL received subcutaneous injection of liraglutide 0.6 mg/kg daily, while C and D received saline for 2 weeks. Afterwards, D and DL received a single intraperitoneal injection of doxorubicin 20 mg/kg; C and L received an injection of saline. Forty-eight hours after doxorubicin administration, the rats were subjected to echocardiogram, isolated heart functional study, and euthanasia. Liraglutide-treated rats ingested significantly less food and gained less body weight than animals that did not receive the drug. Rats lost weight after doxorubicin injection. At echocardiogram and isolated heart study, doxorubicin-treated rats had systolic and diastolic function impairment. Myocardial catalase activity was statistically higher in doxorubicin-treated rats. Myocardial protein expression of tumor necrosis factor alpha (TNF-α), phosphorylated nuclear factor-κB (p-NFκB), troponin T, and B-cell lymphoma 2 (Bcl-2) was significantly lower, and the total NFκB/p-NFκB ratio and TLR-4 higher in doxorubicin-treated rats. Myocardial expression of OPA-1, MFN-2, DRP-1, and topoisomerase 2β did not differ between groups (p > 0.05). In conclusion, doxorubicin-induced cardiotoxicity is accompanied by decreased Bcl-2 and phosphorylated NFκB and increased catalase activity and TLR-4 expression. Liraglutide failed to improve acute doxorubicin-induced cardiotoxicity in rats. Full article
(This article belongs to the Special Issue Heart Failure Mechanisms and Treatment Advances)
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Review

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15 pages, 833 KiB  
Review
Mitochondrial Dysfunction in Heart Failure: From Pathophysiological Mechanisms to Therapeutic Opportunities
by Giovanna Gallo, Speranza Rubattu and Massimo Volpe
Int. J. Mol. Sci. 2024, 25(5), 2667; https://doi.org/10.3390/ijms25052667 - 25 Feb 2024
Cited by 8 | Viewed by 2864
Abstract
Mitochondrial dysfunction, a feature of heart failure, leads to a progressive decline in bioenergetic reserve capacity, consisting in a shift of energy production from mitochondrial fatty acid oxidation to glycolytic pathways. This adaptive process of cardiomyocytes does not represent an effective strategy to [...] Read more.
Mitochondrial dysfunction, a feature of heart failure, leads to a progressive decline in bioenergetic reserve capacity, consisting in a shift of energy production from mitochondrial fatty acid oxidation to glycolytic pathways. This adaptive process of cardiomyocytes does not represent an effective strategy to increase the energy supply and to restore the energy homeostasis in heart failure, thus contributing to a vicious circle and to disease progression. The increased oxidative stress causes cardiomyocyte apoptosis, dysregulation of calcium homeostasis, damage of proteins and lipids, leakage of mitochondrial DNA, and inflammatory responses, finally stimulating different signaling pathways which lead to cardiac remodeling and failure. Furthermore, the parallel neurohormonal dysregulation with angiotensin II, endothelin-1, and sympatho-adrenergic overactivation, which occurs in heart failure, stimulates ventricular cardiomyocyte hypertrophy and aggravates the cellular damage. In this review, we will discuss the pathophysiological mechanisms related to mitochondrial dysfunction, which are mainly dependent on increased oxidative stress and perturbation of the dynamics of membrane potential and are associated with heart failure development and progression. We will also provide an overview of the potential implication of mitochondria as an attractive therapeutic target in the management and recovery process in heart failure. Full article
(This article belongs to the Special Issue Heart Failure Mechanisms and Treatment Advances)
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