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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: 30 June 2024 | Viewed by 1774

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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

Published Papers (3 papers)

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Research

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://0-doi-org.brum.beds.ac.uk/10.3390/ijms25084312 - 13 Apr 2024

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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://0-doi-org.brum.beds.ac.uk/10.3390/ijms25063466 - 19 Mar 2024

Viewed by 598

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://0-doi-org.brum.beds.ac.uk/10.3390/ijms25063268 - 13 Mar 2024

Viewed by 542

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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