International Journal of Molecular Sciences

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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

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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.

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Keywords

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

Published Papers (2 papers)

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Research

Jump to: Review

20 pages, 1734 KiB

Open AccessArticle

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 150

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. 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)

Review

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15 pages, 833 KiB

Open AccessReview

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 1 | Viewed by 1372

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 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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