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Research Progress on the Mechanism and Treatment of Cardiomyopathy: Second Edition

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: 20 November 2025 | Viewed by 1779

Special Issue Editor

Prof. Dr. Michael T. Chin

E-Mail Website
Guest Editor
Molecular Cardiology Research Institute, Tufts Medical Center, Boston, MA 02145, USA
Interests: inherited cardiomyopathies; heart failure; cardiac hypertrophy; gene expression; genetics; molecular biology; single cell transcriptomics; spatial transcriptomics; proteomics; metabolomics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Heart failure is a growing public health problem worldwide that is usually attributable to alterations in cardiac muscle function due to cardiomyopathic processes. Cardiomyopathies have diverse origins, being inherited via gene dysfunction or acquired due to various systemic disorders that manifest in heart dysfunction. Consequently, the pathogenic and molecular mechanisms that promote cardiomyopathic dysfunction are diverse and extensive. Myocardial ischemia resulting from atherosclerotic disease is by far the most frequent cause of myocardial dysfunction, but metabolic, infectious, and inflammatory disorders are also known to result in cardiomyopathy. Alterations in transcription, signaling, mitochondrial function, metabolism, cellular architecture, immune cell function, autophagy, chaperone function and other processes have been implicated at the cellular and molecular levels. Strategies to treat cardiomyopathies range from treating the underlying causes to identifying general strategies for improving systolic and diastolic function. Understanding the mechanisms behind and treatments for various cardiomyopathies will provide wide-ranging insights into the mechanisms of cardiovascular homeostasis and provide opportunities for novel and improved therapeutic targeting.

Prof. Dr. Michael T. Chin
Guest Editor

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Keywords

  • cardiomyopathy
  • heart failure
  • cardiac hypertrophy
  • dilated cardiomyopathy
  • restrictive cardiomyopathy
  • hypertrophic cardiomyopathy
  • ischemic cardiomyopathy
  • viral cardiomyopathy
  • inherited cardiomyopathy

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Related Special Issue

Published Papers (3 papers)

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Research

18 pages, 5783 KiB  
Article
Integrated MicroRNA–mRNA Sequencing Analysis Identifies Regulators and Networks Involved in Feline Hypertrophic Cardiomyopathy
by Jessica Joshua, Jeff L. Caswell, Anja Kipar, M. Lynne O’Sullivan, Geoffrey Wood and Sonja Fonfara
Int. J. Mol. Sci. 2025, 26(14), 6764; https://doi.org/10.3390/ijms26146764 - 15 Jul 2025
Viewed by 114
Abstract
Cardiac remodeling in feline hypertrophic cardiomyopathy (HCM) is poorly understood. To investigate underlying molecular mechanisms, we determined microRNA–mRNA interactions, regulatory networks, and upstream regulators using left ventricle (LV) and left atrium (LA) mRNA and microRNA sequencing datasets from cats with HCM and controls. [...] Read more.
Cardiac remodeling in feline hypertrophic cardiomyopathy (HCM) is poorly understood. To investigate underlying molecular mechanisms, we determined microRNA–mRNA interactions, regulatory networks, and upstream regulators using left ventricle (LV) and left atrium (LA) mRNA and microRNA sequencing datasets from cats with HCM and controls. Upstream regulators, molecules, and pathways associated with ischemia, inflammation, fibrosis, and cellular changes were observed in the HCM heart. In both the HCM LV and LA, TNFα, IL1β, and TGFβ were identified as upstream regulators, along with FGF23, THBS4, and FAMB177 as the top increased molecules. Relevant microRNAs included upstream regulator miR-132, enriched miR-124-3p, miR-122b-3p, miR-146-5p (HCM LV and LA), miR-370, miR-1185-5p, miR-12194-3p (HCM LV), miR-153-3p, miR-185-5p, and miR-185-3p (HCM LA). Macrophage pathways were activated, and granulocyte and agranulocyte adhesion and diapedesis were the most connected pathways. The HIF1α signaling pathway in the HCM LV, upstream regulators miR-1-3p and miR-204, and reduced miR-29 and miR-122-5p suggest cardioprotective mechanisms. Observed in the healthy heart and suspected to be involved in cardiac homeostasis were upstream regulators miR-96, inhibited WNT3A and miR-145, as well as miR-140-5p, miR-141-3p, miR-208b-3p, and miR-885-3p. This study provides further insights into the pathogenesis of HCM, and identifies the factors involved in the maintenance of a healthy LV and LA. Full article
(This article belongs to the Special Issue Research Progress on the Mechanism and Treatment of Cardiomyopathy: Second Edition)
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24 pages, 5181 KiB  
Article
Selected Pathway Analyses to Gain Mechanistic Insights into the Pathogenesis of Feline Hypertrophic Cardiomyopathy
by Lea Schurna, Jessica Joshua, Josep Monné Rodríguez, Francesco Prisco, Marco Baron Toaldo, Simon De Neck, Francesca Baggio, Sonja Fonfara and Anja Kipar
Int. J. Mol. Sci. 2025, 26(13), 6497; https://doi.org/10.3390/ijms26136497 - 5 Jul 2025
Viewed by 319
Abstract
Hypertrophic cardiomyopathy (HCM) is the most prevalent acquired heart disease in cats and shares many clinical, phenotypical and pathological features with human HCM. Despite its relevance, knowledge on the pathomechanisms underlying the disease is limited. The present study aimed to characterize the molecular [...] Read more.
Hypertrophic cardiomyopathy (HCM) is the most prevalent acquired heart disease in cats and shares many clinical, phenotypical and pathological features with human HCM. Despite its relevance, knowledge on the pathomechanisms underlying the disease is limited. The present study aimed to characterize the molecular phenotypic changes in cardiomyocytes in feline HCM (fHCM) to better understand their contribution to the pathogenesis. To achieve this, the myocardium of the left ventricular free wall of 15 cats with confirmed fHCM and 30 control cats (two age groups: 16 cats 18-month-old, and 14 older adult cats without cardiac disease) were subjected to RT-qPCRs for markers representative of cardiomyocyte function. Overall, all markers were expressed at the highest level in young control cats, and increasing age correlated with decreased expression, regardless of sex. The comparison between the older adult control cats and those with HCM showed increased transcription levels for most markers associated with the disease, and higher expression of all markers in affected male cats compared to females. The constitutive transcription of all markers provides evidence of continuous myocardial adaptation throughout cats’ life. The high transcription values in the myocardium of young healthy cats and male cats affected by HCM suggest a particularly high myocardial responsiveness early in life and with HCM and reveal sex as relevant factor in the disease process. These results support the relevance of age and sex in the cardiac response to HCM in feline hearts. Full article
(This article belongs to the Special Issue Research Progress on the Mechanism and Treatment of Cardiomyopathy: Second Edition)
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24 pages, 8284 KiB  
Article
Hypertrophic Cardiomyopathy-Associated CRYABR123W Activates Calcineurin, Reduces Calcium Sequestration, and Alters the CRYAB Interactome and the Proteomic Response to Pathological Hypertrophy
by Andres Thorkelsson, Chun Chou, Audrey Tripp, Samia A. Ali, Jonas Galper and Michael T. Chin
Int. J. Mol. Sci. 2025, 26(6), 2383; https://doi.org/10.3390/ijms26062383 - 7 Mar 2025
Viewed by 1020
Abstract
Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiovascular condition in the world, affecting around 1 in 500 people. HCM is characterized by ventricular wall thickening, decreased ventricular chamber volume, and diastolic dysfunction. Inherited HCM is most commonly caused by sarcomere gene mutations; [...] Read more.
Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiovascular condition in the world, affecting around 1 in 500 people. HCM is characterized by ventricular wall thickening, decreased ventricular chamber volume, and diastolic dysfunction. Inherited HCM is most commonly caused by sarcomere gene mutations; however, approximately 50% of patients do not present with a known mutation, highlighting the need for further research into additional pathological mutations. The alpha-B crystallin (CRYAB) mutation CRYABR123W was previously identified as a novel sarcomere-independent mutation causing HCM associated with pathological NFAT signaling in the setting of pressure overload. We generated stable H9C2 cell lines expressing FLAG-tagged wild-type and mutant CRYAB, which demonstrated that CRYABR123W increases calcineurin activity. Using AlphaFold to predict structural and interaction changes, we generated a model where CRYABR123W uniquely binds to the autoinhibitory domain of calcineurin. Co-immunoprecipitation using the CRYAB FLAG tag followed by mass spectrometry showed novel and distinct changes in the protein interaction patterns of CRYABR123W. Finally, mouse heart extracts from our wild-type CRYAB and CRYABR123W models with and without pressure overload caused by transverse aortic constriction (TAC) were used in global proteomic and phosphoproteomic mass spectrometry analysis, which showed dysregulation in cytoskeletal, metabolomic, cardiac, and immune function. Our data illustrate how CRYABR123W drives calcineurin activation and exhibits distinct changes in protein interaction and cellular pathways during the development of HCM and pathological cardiac hypertrophy. Full article
(This article belongs to the Special Issue Research Progress on the Mechanism and Treatment of Cardiomyopathy: Second Edition)
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