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Breakthroughs in Cardiac Tissue Remodeling: From Mechanisms to Therapeutics

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Guest Editor
Department of Medicine, University of Murcia, 30120 Murcia, Spain
Interests: myocardial infarction; adverse remodeling; heart failure; cardiotoxicity; cardiac dysfunction; ventricular remodeling; cardioprotection; ischemic heart disease; cardiomyopathy; cardiac regeneration
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue “Breakthroughs in Cardiac Tissue Remodeling: From Mechanisms to Therapeutics” will present a selection of recent research topics and current review articles in the field of cardiac tissue remodeling, as well as experimental papers, up-to-date review articles, and commentaries.

Cardiac tissue remodeling plays a pivotal role in the progression of various cardiovascular diseases, including myocardial infarction, heart failure, and cardiomyopathies. Understanding the mechanisms of adverse remodeling and developing strategies to mitigate its effects are critical for improving patient outcomes. Recent research has provided significant insights into the molecular and cellular processes underlying cardiac remodeling, including the roles of inflammation, fibrosis, and neurohormonal activation. Additionally, emerging therapies aim to promote favorable remodeling and restore cardiac function. This Special Issue will highlight advances in several key areas: the molecular and cellular mechanisms driving adverse cardiac remodeling, novel biomarkers for early detection and monitoring, therapeutic interventions targeting remodeling pathways, the impact of cardiotoxicity on cardiac structure and function, and the development of innovative models to study cardiac dysfunction and regeneration. We invite contributions that explore these themes, offering new perspectives on the pathophysiology of cardiac remodeling and potential therapeutic approaches. The goal is to provide a comprehensive overview of current progress and future directions in the field.

Dr. Antonio Lax
Guest Editor

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Keywords

  • myocardial infarction
  • heart failure
  • adverse remodeling
  • cardiac fibrosis
  • cardiomyopathy
  • cardiotoxicity
  • ventricular remodeling
  • cardiac dysfunction
  • biomarkers
  • cardiac regeneration

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Published Papers (1 paper)

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Research

19 pages, 20178 KiB  
Article
Cardiac MRI Strain as an Early Indicator of Myocardial Dysfunction in Hypertrophic Cardiomyopathy
by Siqin Liu, Oumaima Laghzali, Shahriar Shalikar, Mara-Camelia Rusu, Lucie Carrier, Thoralf Niendorf and Min-Chi Ku
Int. J. Mol. Sci. 2025, 26(4), 1407; https://doi.org/10.3390/ijms26041407 - 7 Feb 2025
Cited by 1 | Viewed by 902
Abstract
Hypertrophic cardiomyopathy (HCM) is often characterized by augmented cardiac contractility, which frequently remains undetectable in its early stages. Emerging evidence suggests that hypercontractility is linked to mitochondrial defects that develop early in HCM progression. However, imaging markers for identifying these early alterations in [...] Read more.
Hypertrophic cardiomyopathy (HCM) is often characterized by augmented cardiac contractility, which frequently remains undetectable in its early stages. Emerging evidence suggests that hypercontractility is linked to mitochondrial defects that develop early in HCM progression. However, imaging markers for identifying these early alterations in myocardial function are lacking. We used cardiac magnetic resonance feature tracking (CMR-FT) to assess myocardial strain in a Mybpc3-knockin (KI) mouse model that mimicked human HCM. While homozygous (HOM) mice exhibited cardiac hypertrophy, heterozygous (HET) mice represented an early, asymptomatic stage of HCM. To explore mitochondrial contributions to hypercontractility, we evaluated mitochondrial integrity via scanning electron microscopy (SEM) and correlated these findings with strain abnormalities. Young HET female, but not male mice exhibited significant torsion abnormalities (p = 0.02), reduced left ventricular global longitudinal strain (LVGLS, p = 0.009), and impaired right ventricular global longitudinal strain (RVGLS, p = 0.035) compared to the controls. Strain abnormalities correlated strongly with mitochondrial morphological alterations, including changes in volume and area distribution (R > 0.7). Abnormal myocardial strain patterns, including torsion and GLS, serve as early markers of HCM and are closely associated with underlying mitochondrial dysfunction. The HET Mybpc3-KI HCM model provides important insights into the initial stages of HCM progression, highlighting strain abnormalities and sex-specific differences to enhance early diagnosis and therapeutic strategies. Full article
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