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Research Progress on the Mechanism and Treatment of Cardiomyopathy

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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 (20 December 2024) | Viewed by 14984

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Prof. Dr. Michael T. Chin

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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
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Dear Colleagues,

Heart failure is a growing public health problem worldwide and is most often 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 leading 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 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

Research Progress on the Mechanism and Treatment of Cardiomyopathy: Second Edition in International Journal of Molecular Sciences (1 article)

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15 pages, 20405 KiB

Open AccessArticle

Relative Quantitation of EFNA1 Expression in Mouse Heart Tissue Histologic Sections Using MALDI-MSI

by Maria Torres, Laura Gruer, Smrithi Valsaraj, Shaun Reece, Jeremy Prokop, Tonya Zeczycki, Cameron Taylor, Taylor Byers, William Cruz, Kim Kew, Lisandra de Castro Braz and Jitka Virag

Int. J. Mol. Sci. 2025, 26(4), 1398; https://doi.org/10.3390/ijms26041398 - 7 Feb 2025

Viewed by 708

Abstract

EFNA1 (ephrinA1), a highly expressed tyrosine kinase receptor-ligand in healthy cardiomyocytes, is reduced following myocardial infarction (MI). A single intramyocardial injection of chimeric EFNA1-Fc at the time of ischemia mitigates the injury in both reperfused and non-reperfused mouse myocardium by reducing apoptosis, necrosis, and inflammation. Recently, we have successfully imaged and qualitatively identified endogenous EFNA1 pre- and post-MI using matrix-assisted laser desorption ionization mass spectrometry imaging (MALDI-MSI) coupled with a time-of-flight mass spectrometer (MALDI/TOF MS). Building on our previous work, we are currently focused on understanding and characterizing EFNA1’s role in cardiac tissue by developing an integrated quantitative method to determine endogenous levels of EFNA1 using MALDI-MSI technologies. Herein, we have optimized a method for the relative quantitation of endogenous tryptic EFNA1 peptides detected in the murine heart as compared with routine western blotting. In healthy myocardium, there was approximately 50 ng of endogenous EFNA1 per section of 9.43 mm³ tissue, or roughly 12 pg/µg of homogenized tissue. MALDI-MSI thus provides a tool for determining the anatomical distribution and relative quantitation of endogenous EFNA1 in cardiac tissue. Future applications of these tools will allow us to investigate the dynamic changes in EFNA1 expression profile that occur in pathological states such as myocardial infarction and upon therapeutic treatments. Full article

(This article belongs to the Special Issue Research Progress on the Mechanism and Treatment of Cardiomyopathy)

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17 pages, 2629 KiB

Open AccessArticle

Novel Mutation Lys30Glu in the TPM1 Gene Leads to Pediatric Left Ventricular Non-Compaction and Dilated Cardiomyopathy via Impairment of Structural and Functional Properties of Cardiac Tropomyosin

by Elena V. Zaklyazminskaya, Victoria V. Nefedova, Natalia A. Koubassova, Natalia P. Kotlukova, Galina V. Kopylova, Anastasia M. Kochurova, Daniil V. Shchepkin, Natalia S. Ryabkova, Ivan A. Katrukha, Sergey Y. Kleymenov, Sergey Y. Bershitsky, Alexander M. Matyushenko, Andrey K. Tsaturyan and Dmitrii I. Levitsky

Int. J. Mol. Sci. 2024, 25(23), 13059; https://doi.org/10.3390/ijms252313059 - 5 Dec 2024

Cited by 1 | Viewed by 1164

Abstract

Pediatric dilated cardiomyopathy (DCM) is a rare heart muscle disorder leading to the enlargement of all chambers and systolic dysfunction. We identified a novel de novo variant, c.88A>G (p.Lys30Glu, K30E), in the TPM1 gene encoding the major cardiac muscle tropomyosin (Tpm) isoform, Tpm1.1. The variant was found in a proband with DCM and left ventricular non-compaction who progressed to terminal heart failure at the age of 3 years and 8 months. To study the properties of the mutant protein, we produced recombinant K30E Tpm and used various biochemical and biophysical methods to compare its properties with those of WT Tpm. The K30E substitution decreased the thermal stability of Tpm and its complex with actin and significantly reduced the sliding velocity of the regulated thin filaments over a surface covered by ovine cardiac myosin in an in vitro motility assay across the entire physiological range of Ca²⁺ concentration. Our molecular dynamics simulations suggest that the charge reversal of the 30th residue of Tpm alters the actin monomer to which it is bound. We hypothesize that this rearrangement of the actin–Tpm interaction may hinder the transition of a myosin head attached to a nearby actin from a weakly to a strongly bound, force-generating state, thereby reducing myocardial contractility. The impaired myosin interaction with regulated actin filaments and the decreased thermal stability of the actin–Tpm complex at a near physiological temperature likely contribute to the pathogenicity of the variant and its causative role in progressive DCM. Full article

(This article belongs to the Special Issue Research Progress on the Mechanism and Treatment of Cardiomyopathy)

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18 pages, 4253 KiB

Open AccessArticle

The D75N and P161S Mutations in the C0-C2 Fragment of cMyBP-C Associated with Hypertrophic Cardiomyopathy Disturb the Thin Filament Activation, Nucleotide Exchange in Myosin, and Actin–Myosin Interaction

by Anastasia M. Kochurova, Evgenia A. Beldiia, Victoria V. Nefedova, Daria S. Yampolskaya, Natalia A. Koubassova, Sergey Y. Kleymenov, Julia Y. Antonets, Natalia S. Ryabkova, Ivan A. Katrukha, Sergey Y. Bershitsky, Alexander M. Matyushenko, Galina V. Kopylova and Daniil V. Shchepkin

Int. J. Mol. Sci. 2024, 25(20), 11195; https://doi.org/10.3390/ijms252011195 - 18 Oct 2024

Cited by 1 | Viewed by 1333

Abstract

About half of the mutations that lead to hypertrophic cardiomyopathy (HCM) occur in the MYBPC3 gene. However, the molecular mechanisms of pathogenicity of point mutations in cardiac myosin-binding protein C (cMyBP-C) remain poorly understood. In this study, we examined the effects of the D75N and P161S substitutions in the C0 and C1 domains of cMyBP-C on the structural and functional properties of the C0-C1-m-C2 fragment (C0-C2). Differential scanning calorimetry revealed that these mutations disorder the tertiary structure of the C0-C2 molecule. Functionally, the D75N mutation reduced the maximum sliding velocity of regulated thin filaments in an in vitro motility assay, while the P161S mutation increased it. Both mutations significantly reduced the calcium sensitivity of the actin–myosin interaction and impaired thin filament activation by cross-bridges. D75N and P161S C0-C2 fragments substantially decreased the sliding velocity of the F-actin-tropomyosin filament. ADP dose-dependently reduced filament sliding velocity in the presence of WT and P161S fragments, but the velocity remained unchanged with the D75N fragment. We suppose that the D75N mutation alters nucleotide exchange kinetics by decreasing ADP affinity to the ATPase pocket and slowing the myosin cycle. Our molecular dynamics simulations mean that the D75N mutation affects myosin S1 function. Both mutations impair cardiac contractility by disrupting thin filament activation. The results offer new insights into the HCM pathogenesis caused by missense mutations in N-terminal domains of cMyBP-C, highlighting the distinct effects of D75N and P161S mutations on cardiac contractile function. Full article

(This article belongs to the Special Issue Research Progress on the Mechanism and Treatment of Cardiomyopathy)

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21 pages, 1682 KiB

Open AccessArticle

Neutrophil Biomarkers Can Predict Cardiotoxicity of Anthracyclines in Breast Cancer

by Valentina K. Todorova, Gohar Azhar, Annjanette Stone, Sindhu J. Malapati, Yingni Che, Wei Zhang, Issam Makhoul and Jeanne Y. Wei

Int. J. Mol. Sci. 2024, 25(17), 9735; https://doi.org/10.3390/ijms25179735 - 9 Sep 2024

Cited by 2 | Viewed by 1542

Abstract

Doxorubicin (DOX), a commonly used anticancer agent, causes cardiotoxicity that begins with the first dose and may progress to heart failure years after treatment. An inflammatory response associated with neutrophil recruitment has been recognized as a mechanism of DOX-induced cardiotoxicity. This study aimed to validate mRNA expression of the previously identified biomarkers of DOX-induced cardiotoxicity, PGLYRP1, CAMP, MMP9, and CEACAM8, and to assay their protein expression in the peripheral blood of breast cancer patients. Blood samples from 40 breast cancer patients treated with DOX-based chemotherapy were collected before and after the first chemotherapy cycle and > 2 years after treatment. The protein and gene expression of PGLYRP1/Tag7, CAMP/LL37, MMP9/gelatinase B, and CEACAM8/CD66b were determined using ELISA and reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Receiver operating characteristic (ROC) curve analysis was used to determine the diagnostic value of each candidate biomarker. Patients with cardiotoxicity (n = 20) had significantly elevated levels of PGLYRP1, CAMP, MMP9, and CEACAM8 at baseline, after the first dose of DOX-based chemotherapy, and at > 2 years after treatment relative to patients without cardiotoxicity (n = 20). The first dose of DOX induced significantly higher levels of all examined biomarkers in both groups of patients. At > 2 years post treatment, the levels of all but MMP9 dropped below the baseline. There was a good correlation between the expression of mRNA and the target proteins. We demonstrate that circulating levels of PGLYRP1, CAMP, MMP9, and CEACAM8 can predict the cardiotoxicity of DOX. This novel finding may be of value in the early identification of patients at risk for cardiotoxicity. Full article

(This article belongs to the Special Issue Research Progress on the Mechanism and Treatment of Cardiomyopathy)

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26 pages, 15088 KiB

Open AccessArticle

A Barth Syndrome Patient-Derived D75H Point Mutation in TAFAZZIN Drives Progressive Cardiomyopathy in Mice

by Paige L. Snider, Elizabeth A. Sierra Potchanant, Zejin Sun, Donna M. Edwards, Ka-Kui Chan, Catalina Matias, Junya Awata, Aditya Sheth, P. Melanie Pride, R. Mark Payne, Michael Rubart, Jeffrey J. Brault, Michael T. Chin, Grzegorz Nalepa and Simon J. Conway

Int. J. Mol. Sci. 2024, 25(15), 8201; https://doi.org/10.3390/ijms25158201 - 27 Jul 2024

Cited by 4 | Viewed by 1984

Abstract

Cardiomyopathy is the predominant defect in Barth syndrome (BTHS) and is caused by a mutation of the X-linked Tafazzin (TAZ) gene, which encodes an enzyme responsible for remodeling mitochondrial cardiolipin. Despite the known importance of mitochondrial dysfunction in BTHS, how specific TAZ mutations cause diverse BTHS heart phenotypes remains poorly understood. We generated a patient-tailored CRISPR/Cas9 knock-in mouse allele (Taz^PM) that phenocopies BTHS clinical traits. As Taz^PM males express a stable mutant protein, we assessed cardiac metabolic dysfunction and mitochondrial changes and identified temporally altered cardioprotective signaling effectors. Specifically, juvenile Taz^PM males exhibit mild left ventricular dilation in systole but have unaltered fatty acid/amino acid metabolism and normal adenosine triphosphate (ATP). This occurs in concert with a hyperactive p53 pathway, elevation of cardioprotective antioxidant pathways, and induced autophagy-mediated early senescence in juvenile Taz^PM hearts. However, adult Taz^PM males exhibit chronic heart failure with reduced growth and ejection fraction, cardiac fibrosis, reduced ATP, and suppressed fatty acid/amino acid metabolism. This biphasic changeover from a mild-to-severe heart phenotype coincides with p53 suppression, downregulation of cardioprotective antioxidant pathways, and the onset of terminal senescence in adult Taz^PM hearts. Herein, we report a BTHS genotype/phenotype correlation and reveal that absent Taz acyltransferase function is sufficient to drive progressive cardiomyopathy. Full article

(This article belongs to the Special Issue Research Progress on the Mechanism and Treatment of Cardiomyopathy)

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12 pages, 2132 KiB

Open AccessArticle

Effect of Low-Level Tragus Stimulation on Cardiac Metabolism in Heart Failure with Preserved Ejection Fraction: A Transcriptomics-Based Analysis

by Praloy Chakraborty, Monika Niewiadomska, Kassem Farhat, Lynsie Morris, Seabrook Whyte, Kenneth M. Humphries and Stavros Stavrakis

Int. J. Mol. Sci. 2024, 25(8), 4312; https://doi.org/10.3390/ijms25084312 - 13 Apr 2024

Viewed by 1584

Abstract

Abnormal cardiac metabolism precedes and contributes to structural changes in heart failure. Low-level tragus stimulation (LLTS) can attenuate structural remodeling in heart failure with preserved ejection fraction (HFpEF). The role of LLTS on cardiac metabolism is not known. Dahl salt-sensitive rats of 7 weeks of age were randomized into three groups: low salt (0.3% NaCl) diet (control group; n = 6), high salt diet (8% NaCl) with either LLTS (active group; n = 8), or sham stimulation (sham group; n = 5). Both active and sham groups received the high salt diet for 10 weeks with active LLTS or sham stimulation (20 Hz, 2 mA, 0.2 ms) for 30 min daily for the last 4 weeks. At the endpoint, left ventricular tissue was used for RNA sequencing and transcriptomic analysis. The Ingenuity Pathway Analysis tool (IPA) was used to identify canonical metabolic pathways and upstream regulators. Principal component analysis demonstrated overlapping expression of important metabolic genes between the LLTS, and control groups compared to the sham group. Canonical metabolic pathway analysis showed downregulation of the oxidative phosphorylation (Z-score: −4.707, control vs. sham) in HFpEF and LLTS improved the oxidative phosphorylation (Z-score = −2.309, active vs. sham). HFpEF was associated with the abnormalities of metabolic upstream regulators, including PPARGC1α, insulin receptor signaling, PPARα, PPARδ, PPARGC1β, the fatty acid transporter SLC27A2, and lysine-specific demethylase 5A (KDM5A). LLTS attenuated abnormal insulin receptor and KDM5A signaling. HFpEF is associated with abnormal cardiac metabolism. LLTS, by modulating the functioning of crucial upstream regulators, improves cardiac metabolism and mitochondrial oxidative phosphorylation. Full article

(This article belongs to the Special Issue Research Progress on the Mechanism and Treatment of Cardiomyopathy)

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17 pages, 12652 KiB

Open AccessArticle

Long Non-Coding RNA-Cardiac-Inducing RNA 6 Mediates Repair of Infarcted Hearts by Inducing Mesenchymal Stem Cell Differentiation into Cardiogenic Cells through Cyclin-Dependent Kinase 1

by Xiaotian Cui, Hui Dong, Shenghe Luo, Bingqi Zhuang, Yansheng Li, Chongning Zhong, Yuting Ma and Lan Hong

Int. J. Mol. Sci. 2024, 25(6), 3466; https://doi.org/10.3390/ijms25063466 - 19 Mar 2024

Cited by 4 | Viewed by 1758

Abstract

This study aims to investigate the induction effect of LncRNA-CIR6 on MSC differentiation into cardiogenic cells in vitro and in vivo. In addition to pretreatment with Ro-3306 (a CDK1 inhibitor), LncRNA-CIR6 was transfected into BMSCs and hUCMSCs using jetPRIME. LncRNA-CIR6 was further transfected into the hearts of C57BL/6 mice via 100 μL of AAV9-cTnT-LncRNA-CIR6-ZsGreen intravenous injection. After three weeks of transfection followed by AMI surgery, hUCMSCs (5 × 10⁵/100 μL) were injected intravenously one week later. Cardiac function was evaluated using VEVO 2100 and electric mapping nine days after cell injection. Immunofluorescence, Evans blue-TTC, Masson staining, FACS, and Western blotting were employed to determine relevant indicators. LncRNA-CIR6 induced a significant percentage of differentiation in BMSCs (83.00 ± 0.58)% and hUCMSCs (95.43 ± 2.13)% into cardiogenic cells, as determined by the expression of cTnT using immunofluorescence and FACS. High cTNT expression was observed in MSCs after transfection with LncRNA-CIR6 by Western blotting. Compared with the MI group, cardiac contraction and conduction function in MI hearts treated with LncRNA-CIR6 or combined with MSCs injection groups were significantly increased, and the areas of MI and fibrosis were significantly lower. The transcriptional expression region of LncRNA-CIR6 was on Chr17 from 80209290 to 80209536. The functional region of LncRNA-CIR6 was located at nucleotides 0–50/190–255 in the sequence. CDK1, a protein found to be related to the proliferation and differentiation of cardiomyocytes, was located in the functional region of the LncRNA-CIR6 secondary structure (from 0 to 17). Ro-3306 impeded the differentiation of MSCs into cardiogenic cells, while MSCs transfected with LncRNA-CIR6 showed a high expression of CDK1. LncRNA-CIR6 mediates the repair of infarcted hearts by inducing MSC differentiation into cardiogenic cells through CDK1. Full article

(This article belongs to the Special Issue Research Progress on the Mechanism and Treatment of Cardiomyopathy)

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16 pages, 5010 KiB

Open AccessArticle

Microcurrent-Mediated Modulation of Myofibroblasts for Cardiac Repair and Regeneration

by Dipthi Bachamanda Somesh, Karsten Jürchott, Thomas Giesel, Thomas Töllner, Alexander Prehn, Jan-Peter Richters, Dragana Kosevic, Jesus Eduardo Rame, Peter Göttel and Johannes Müller

Int. J. Mol. Sci. 2024, 25(6), 3268; https://doi.org/10.3390/ijms25063268 - 13 Mar 2024

Cited by 3 | Viewed by 1895

Abstract

Cardiovascular diseases are a significant cause of illness and death worldwide, often resulting in myofibroblast differentiation, pathological remodeling, and fibrosis, characterized by excessive extracellular matrix protein deposition. Treatment options for cardiac fibrosis that can effectively target myofibroblast activation and ECM deposition are limited, necessitating an unmet need for new therapeutic approaches. In recent years, microcurrent therapy has demonstrated promising therapeutic effects, showcasing its translational potential in cardiac care. This study therefore sought to investigate the effects of microcurrent therapy on cardiac myofibroblasts, aiming to unravel its potential as a treatment for cardiac fibrosis and heart failure. The experimental design involved the differentiation of primary rat cardiac fibroblasts into myofibroblasts. Subsequently, these cells were subjected to microcurrent (MC) treatment at 1 and 2 µA/cm² DC with and without polarity reversal. We then investigated the impact of microcurrent treatment on myofibroblast cell behavior, including protein and gene expression, by performing various assays and analyses comparing them to untreated myofibroblasts and cardiac fibroblasts. The application of microcurrents resulted in distinct transcriptional signatures and improved cellular processes. Gene expression analysis showed alterations in myofibroblast markers, extracellular matrix components, and pro-inflammatory cytokines. These observations show signs of microcurrent-mediated reversal of myofibroblast phenotype, possibly reducing cardiac fibrosis, and providing insights for cardiac tissue repair. Full article

(This article belongs to the Special Issue Research Progress on the Mechanism and Treatment of Cardiomyopathy)

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Review

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Open AccessReview

Dynamic Changes in Ion Channels during Myocardial Infarction and Therapeutic Challenges

by Tongtong Song, Wenting Hui, Min Huang, Yan Guo, Meiyi Yu, Xiaoyu Yang, Yanqing Liu and Xia Chen

Int. J. Mol. Sci. 2024, 25(12), 6467; https://doi.org/10.3390/ijms25126467 - 12 Jun 2024

Cited by 2 | Viewed by 2120

Abstract

In different areas of the heart, action potential waveforms differ due to differences in the expressions of sodium, calcium, and potassium channels. One of the characteristics of myocardial infarction (MI) is an imbalance in oxygen supply and demand, leading to ion imbalance. After MI, the regulation and expression levels of K⁺, Ca²⁺, and Na⁺ ion channels in cardiomyocytes are altered, which affects the regularity of cardiac rhythm and leads to myocardial injury. Myocardial fibroblasts are the main effector cells in the process of MI repair. The ion channels of myocardial fibroblasts play an important role in the process of MI. At the same time, a large number of ion channels are expressed in immune cells, which play an important role by regulating the in- and outflow of ions to complete intracellular signal transduction. Ion channels are widely distributed in a variety of cells and are attractive targets for drug development. This article reviews the changes in different ion channels after MI and the therapeutic drugs for these channels. We analyze the complex molecular mechanisms behind myocardial ion channel regulation and the challenges in ion channel drug therapy. Full article

(This article belongs to the Special Issue Research Progress on the Mechanism and Treatment of Cardiomyopathy)

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