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Molecular Mechanisms of Myocardial Injury and Repair

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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 (31 October 2023) | Viewed by 6597

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Special Issue Editors

Dr. Jason Peart

E-Mail Website
Guest Editor

School of Pharmacy and Medical Science, Griffith University, Southport, QLD 4217, Australia
Interests: ischemia-reperfusion; cardioprotection; infarction; co-morbidities
Special Issues, Collections and Topics in MDPI journals

Dr. Louise E. See Hoe

E-Mail Website
Guest Editor

Critical Care Research Group, The Prince Charles Hospital, Chermside, QLD 4032, Australia
Interests: cardioprotection; cardiac ischemia-reperfusion injury

Special Issue Information

Dear Colleagues,

The understanding and ongoing discovery of the molecular mechanisms of myocardial injury and repair is both fascinating and complex. Disease states such as aging and diabetes not only lead to myocardial modifications and damage, they may exacerbate injury due to stressors such as ischemia and reperfusion. Counter to this, neonatal hearts exhibit a profound capacity for repair; however, this innate reparative function is rapidly lost with maturation. Mechanisms impacting myocardial injury and repair, particularly in the setting of co-morbidities are complex in nature and a challenge to delineate, likely in part due to the different cell types present in the heart and the nature of co-morbidities. In recent years, we have seen a rapid expansion of depth in the field based on new technologies. For example, single cell sequencing and the explosion of microRNA analysis have afforded a much deeper and distinct understanding of how pathological states drive myocardial injury, markers for the detection of injury and molecular pathways to harness for repair. The purpose of this Special Issue is to gather the latest information and highlight the state of the art in the progress of the molecular mechanisms of myocardial injury and repair with a focus on, but not limited to, the impact of relevant comorbidities.

We invite exemplar reviews, commentaries, and original research articles based on cutting-edge technology as well as those from more classic biochemical, molecular, and cellular approaches.

Dr. Jason Peart
Dr. Louise E. See Hoe
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

myocardial injury
myocardial repair
ischemia-reperfusion
hypertrophy
fibrosis
infarction
co-morbidities

Published Papers (3 papers)

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Research

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16 pages, 2577 KiB

Open AccessArticle

Extracellular Histone-Induced Protein Kinase C Alpha Activation and Troponin Phosphorylation Is a Potential Mechanism of Cardiac Contractility Depression in Sepsis

by Simon T. Abrams, Yasir Alhamdi, Min Zi, Fengmei Guo, Min Du, Guozheng Wang, Elizabeth J. Cartwright and Cheng-Hock Toh

Int. J. Mol. Sci. 2023, 24(4), 3225; https://doi.org/10.3390/ijms24043225 - 6 Feb 2023

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Abstract

Reduction in cardiac contractility is common in severe sepsis. However, the pathological mechanism is still not fully understood. Recently it has been found that circulating histones released after extensive immune cell death play important roles in multiple organ injury and disfunction, particularly in cardiomyocyte injury and contractility reduction. How extracellular histones cause cardiac contractility depression is still not fully clear. In this work, using cultured cardiomyocytes and a histone infusion mouse model, we demonstrate that clinically relevant histone concentrations cause significant increases in intracellular calcium concentrations with subsequent activation and enriched localization of calcium-dependent protein kinase C (PKC) α and βII into the myofilament fraction of cardiomyocytes in vitro and in vivo. Furthermore, histones induced dose-dependent phosphorylation of cardiac troponin I (cTnI) at the PKC-regulated phosphorylation residues (S43 and T144) in cultured cardiomyocytes, which was also confirmed in murine cardiomyocytes following intravenous histone injection. Specific inhibitors against PKCα and PKCβII revealed that histone-induced cTnI phosphorylation was mainly mediated by PKCα activation, but not PKCβII. Blocking PKCα also significantly abrogated histone-induced deterioration in peak shortening, duration and the velocity of shortening, and re-lengthening of cardiomyocyte contractility. These in vitro and in vivo findings collectively indicate a potential mechanism of histone-induced cardiomyocyte dysfunction driven by PKCα activation with subsequent enhanced phosphorylation of cTnI. These findings also indicate a potential mechanism of clinical cardiac dysfunction in sepsis and other critical illnesses with high levels of circulating histones, which holds the potential translational benefit to these patients by targeting circulating histones and downstream pathways. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Myocardial Injury and Repair)

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14 pages, 2977 KiB

Open AccessArticle

Meta-Analysis of Extracellular Matrix Dynamics after Myocardial Infarction Using RNA-Sequencing Transcriptomic Database

by María Ortega, César Ríos-Navarro, Jose Gavara, Elena de Dios, Nerea Perez-Solé, Victor Marcos-Garcés, Antonio Ferrández-Izquierdo, Vicente Bodí and Amparo Ruiz-Saurí

Int. J. Mol. Sci. 2022, 23(24), 15615; https://doi.org/10.3390/ijms232415615 - 9 Dec 2022

Cited by 2 | Viewed by 1963

Abstract

Extracellular matrix (ECM) changes after myocardial infarction (MI) need precise regulation, and next-generation sequencing technologies provide omics data that can be used in this context. We performed a meta-analysis using RNA-sequencing transcriptomic datasets to identify genes involved in post-MI ECM turnover. Eight studies available in Gene Expression Omnibus were selected following the inclusion criteria. We compare RNA-sequencing data from 92 mice submitted to permanent coronary ligation or sham, identifying differentially expressed genes (p-value < 0.05 and Log2FoldChange ≥ 2). Functional enrichment analysis was performed based on Gene Ontology biological processes (BPs). BPs implicated in response to extracellular stimulus, regulation of ECM organization, and ECM disassembly were detected soon after ischemia onset. ECM disassembly occurred between days one to seven post-MI, compared with ECM assembly from day seven onwards. We identified altered mRNA expression of 19 matrix metalloproteinases and four tissue inhibitors of metalloproteinases at post-infarcted ECM remodeling and altered transcriptomic expression of 42 genes encoding 26 collagen subunits at the fibrotic stage. To our knowledge, this is the first meta-analysis using RNA-sequencing datasets to evaluate post-infarcted cardiac interstitium healing, revealing previously unknown mechanisms and molecules actively implicated in ECM remodeling post-MI, which warrant further validation. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Myocardial Injury and Repair)

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Review

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14 pages, 2290 KiB

Open AccessReview

The Protective Role of TREM2 in the Heterogenous Population of Macrophages during Post-Myocardial Infarction Inflammation

by Sang Hyun Kim, Kwan Yong Lee and Kiyuk Chang

Int. J. Mol. Sci. 2023, 24(6), 5556; https://doi.org/10.3390/ijms24065556 - 14 Mar 2023

Cited by 3 | Viewed by 2760

Abstract

Advances in interventions after myocardial infarction (MI) have dramatically increased survival, but MI remains the leading cause of heart failure due to maladaptive ventricular remodeling following ischemic damage. Inflammation is crucial in both the initial response to ischemia and subsequent wound healing in the myocardium. To date, preclinical and clinical efforts have been made to elucidate the deleterious effects of immune cells contributing to ventricular remodeling and to identify therapeutic molecular targets. The conventional concept classifies macrophages or monocytes into dichotomous populations, while recent studies support their diverse subpopulations and spatiotemporal dynamicity. The single-cell and spatial transcriptomic landscapes of macrophages in infarcted hearts successfully revealed the heterogeneity of cell types and their subpopulations post-MI. Among them, subsets of Trem2^hi macrophages were identified that were recruited to infarcted myocardial tissue in the subacute phase of MI. The upregulation of anti-inflammatory genes was observed in Trem2^hi macrophages, and an in vivo injection of soluble Trem2 during the subacute phase of MI significantly improved myocardial function and the remodeling of infarcted mice hearts, suggesting the potential therapeutic role of Trem2 in LV remodeling. Further investigation of the reparative role of Trem2 in LV remodeling would provide novel therapeutic targets for MI. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Myocardial Injury and Repair)

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