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Cells
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Mechanisms of Ischemic Heart Injury
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Mechanisms of Ischemic Heart Injury

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Cardiovascular System".

Deadline for manuscript submissions: closed (10 December 2021) | Viewed by 38601

Special Issue Editor

Prof. Dominic P. Del Re

E-Mail Website
Guest Editor
Department of Cell Biology and Molecular Medicine, Rutgers, New Jersey Medical School, 185 South Orange Avenue, Newark, NJ 07103, USA
Interests: myocardial infarction; heart failure; regulated cell death; Hippo pathway

Special Issue Information

Dear Colleagues,

Cardiovascular disease remains a leading cause of morbidity and mortality worldwide, as well as an enormous global economic burden. Myocardial infarction, primarily the result of coronary artery disease, elicits massive cardiomyocyte loss and irreparable damage to heart muscle, leading to impaired cardiac function and heart failure. The current standard of care to treat patients suffering myocardial infarction—typically primary percutaneous coronary intervention to allow myocardial reperfusion—limits the loss of viable myocardium. Paradoxically however, timely intervention does not prevent the additional tissue damage resulting from the act of reperfusion itself, which may contribute to injury and worsen outcomes. An incomplete understanding of the mechanisms underlying myocardial ischemia and reperfusion injury remains a significant barrier to improved therapeutics to mitigate cardiac damage.

This Special Issue aims to summarize the current knowledge related to ischemic heart injury, and to enhance our understanding of basic mechanisms underlying this phenomenon, with the hope of advancing the field toward novel potential therapeutic strategies to improve patient outcomes.

We look forward to your contribution to this Special Issue of Cells.

Prof. Dominic P. Del Re
Guest Editor

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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • heart failure
  • myocardial infarction
  • ischemia
  • reperfusion
  • cardiomyocyte
  • cell death
  • cardioprotection

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Published Papers (8 papers)

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Editorial

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3 pages, 173 KiB  
Editorial
Mechanisms of Ischemic Heart Injury
by Dominic P. Del Re
Cells 2022, 11(9), 1384; https://doi.org/10.3390/cells11091384 - 19 Apr 2022
Cited by 4 | Viewed by 1792
Abstract
Ischemic heart disease is a leading cause of morbidity and mortality worldwide [...] Full article
(This article belongs to the Special Issue Mechanisms of Ischemic Heart Injury)

Research

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16 pages, 3071 KiB  
Article
Tfeb-Mediated Transcriptional Regulation of Autophagy Induces Autosis during Ischemia/Reperfusion in the Heart
by Jihoon Nah, Eun-Ah Sung, Peiyong Zhai, Daniela Zablocki and Junichi Sadoshima
Cells 2022, 11(2), 258; https://doi.org/10.3390/cells11020258 - 13 Jan 2022
Cited by 15 | Viewed by 3301
Abstract
Autosis is a unique form of cell death with characteristic morphological and biochemical features caused by dysregulated autophagy. Autosis is observed in the heart during the late phase of ischemia/reperfusion (I/R), when marked accumulation of autophagosomes is induced. We previously showed that the [...] Read more.
Autosis is a unique form of cell death with characteristic morphological and biochemical features caused by dysregulated autophagy. Autosis is observed in the heart during the late phase of ischemia/reperfusion (I/R), when marked accumulation of autophagosomes is induced. We previously showed that the excessive accumulation of autophagosomes promotes autosis in cardiomyocytes. Although the inhibition of autophagic flux via the upregulation of Rubicon induces the accumulation of autophagosomes during I/R, it appears that additional mechanisms exacerbating autophagosome accumulation are required for the induction of autosis. Here, we show that Tfeb contributes to the induction of autosis during the late phase of I/R in the heart. During myocardial reperfusion, Tfeb is activated and translocated into the nucleus, which in turn upregulates genes involved in autophagy and lysosomal function. The overexpression of Tfeb enhanced cardiomyocyte death induced by a high dose of TAT-Beclin 1, an effect that was inhibited by the downregulation of Atg7. Conversely, the knockdown of Tfeb attenuated high-dose TAT-Beclin1-induced death in cardiomyocytes. Although the downregulation of Tfeb in the heart significantly decreased the number of autophagic vacuoles and inhibited autosis during I/R, the activation of Tfeb activity via 3,4-dimethoxychalcone, an activator of Tfeb, aggravated myocardial injury during I/R. These findings suggest that Tfeb promotes cardiomyocyte autosis during the late phase of reperfusion in the heart. Full article
(This article belongs to the Special Issue Mechanisms of Ischemic Heart Injury)
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19 pages, 5926 KiB  
Article
Deep Learning Analyses to Delineate the Molecular Remodeling Process after Myocardial Infarction
by Oriol Iborra-Egea, Carolina Gálvez-Montón, Cristina Prat-Vidal, Santiago Roura, Carolina Soler-Botija, Elena Revuelta-López, Gemma Ferrer-Curriu, Cristina Segú-Vergés, Araceli Mellado-Bergillos, Pol Gomez-Puchades, Paloma Gastelurrutia and Antoni Bayes-Genis
Cells 2021, 10(12), 3268; https://doi.org/10.3390/cells10123268 - 23 Nov 2021
Cited by 2 | Viewed by 2985
Abstract
Specific proteins and processes have been identified in post-myocardial infarction (MI) pathological remodeling, but a comprehensive understanding of the complete molecular evolution is lacking. We generated microarray data from swine heart biopsies at baseline and 6, 30, and 45 days after infarction to [...] Read more.
Specific proteins and processes have been identified in post-myocardial infarction (MI) pathological remodeling, but a comprehensive understanding of the complete molecular evolution is lacking. We generated microarray data from swine heart biopsies at baseline and 6, 30, and 45 days after infarction to feed machine-learning algorithms. We cross-validated the results using available clinical and experimental information. MI progression was accompanied by the regulation of adipogenesis, fatty acid metabolism, and epithelial–mesenchymal transition. The infarct core region was enriched in processes related to muscle contraction and membrane depolarization. Angiogenesis was among the first morphogenic responses detected as being sustained over time, but other processes suggesting post-ischemic recapitulation of embryogenic processes were also observed. Finally, protein-triggering analysis established the key genes mediating each process at each time point, as well as the complete adverse remodeling response. We modeled the behaviors of these genes, generating a description of the integrative mechanism of action for MI progression. This mechanistic analysis overlapped at different time points; the common pathways between the source proteins and cardiac remodeling involved IGF1R, RAF1, KPCA, JUN, and PTN11 as modulators. Thus, our data delineate a structured and comprehensive picture of the molecular remodeling process, identify new potential biomarkers or therapeutic targets, and establish therapeutic windows during disease progression. Full article
(This article belongs to the Special Issue Mechanisms of Ischemic Heart Injury)
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Review

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35 pages, 2321 KiB  
Review
An Overview of the Molecular Mechanisms Associated with Myocardial Ischemic Injury: State of the Art and Translational Perspectives
by Leonardo Schirone, Maurizio Forte, Luca D’Ambrosio, Valentina Valenti, Daniele Vecchio, Sonia Schiavon, Giulia Spinosa, Gianmarco Sarto, Vincenzo Petrozza, Giacomo Frati and Sebastiano Sciarretta
Cells 2022, 11(7), 1165; https://doi.org/10.3390/cells11071165 - 30 Mar 2022
Cited by 44 | Viewed by 11405
Abstract
Cardiovascular disease is the leading cause of death in western countries. Among cardiovascular diseases, myocardial infarction represents a life-threatening condition predisposing to the development of heart failure. In recent decades, much effort has been invested in studying the molecular mechanisms underlying the development [...] Read more.
Cardiovascular disease is the leading cause of death in western countries. Among cardiovascular diseases, myocardial infarction represents a life-threatening condition predisposing to the development of heart failure. In recent decades, much effort has been invested in studying the molecular mechanisms underlying the development and progression of ischemia/reperfusion (I/R) injury and post-ischemic cardiac remodeling. These mechanisms include metabolic alterations, ROS overproduction, inflammation, autophagy deregulation and mitochondrial dysfunction. This review article discusses the most recent evidence regarding the molecular basis of myocardial ischemic injury and the new potential therapeutic interventions for boosting cardioprotection and attenuating cardiac remodeling. Full article
(This article belongs to the Special Issue Mechanisms of Ischemic Heart Injury)
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13 pages, 1094 KiB  
Review
Functional Role of microRNAs in Regulating Cardiomyocyte Death
by Urna Kansakar, Fahimeh Varzideh, Pasquale Mone, Stanislovas S. Jankauskas and Gaetano Santulli
Cells 2022, 11(6), 983; https://doi.org/10.3390/cells11060983 - 12 Mar 2022
Cited by 30 | Viewed by 4109
Abstract
microRNAs (miRNA, miRs) play crucial roles in cardiovascular disease regulating numerous processes, including inflammation, cell proliferation, angiogenesis, and cell death. Herein, we present an updated and comprehensive overview of the functional involvement of miRs in the regulation of cardiomyocyte death, a central event [...] Read more.
microRNAs (miRNA, miRs) play crucial roles in cardiovascular disease regulating numerous processes, including inflammation, cell proliferation, angiogenesis, and cell death. Herein, we present an updated and comprehensive overview of the functional involvement of miRs in the regulation of cardiomyocyte death, a central event in acute myocardial infarction, ischemia/reperfusion, and heart failure. Specifically, in this systematic review we are focusing on necrosis, apoptosis, and autophagy. Full article
(This article belongs to the Special Issue Mechanisms of Ischemic Heart Injury)
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15 pages, 1253 KiB  
Review
Novel Techniques Targeting Fibroblasts after Ischemic Heart Injury
by Sirin N. Cakir, Kaitlin M. Whitehead, Hanifah K. L. Hendricks and Lisandra E. de Castro Brás
Cells 2022, 11(3), 402; https://doi.org/10.3390/cells11030402 - 25 Jan 2022
Cited by 6 | Viewed by 6243
Abstract
The great plasticity of cardiac fibroblasts allows them to respond quickly to myocardial injury and to contribute to the subsequent cardiac remodeling. Being the most abundant cell type (in numbers) in the heart, and a key participant in the several phases of tissue [...] Read more.
The great plasticity of cardiac fibroblasts allows them to respond quickly to myocardial injury and to contribute to the subsequent cardiac remodeling. Being the most abundant cell type (in numbers) in the heart, and a key participant in the several phases of tissue healing, the cardiac fibroblast is an excellent target for treating cardiac diseases. The development of cardiac fibroblast-specific approaches have, however, been difficult due to the lack of cellular specific markers. The development of genetic lineage tracing tools and Cre-recombinant transgenics has led to a huge acceleration in cardiac fibroblast research. Additionally, the use of novel targeted delivery approaches like nanoparticles and modified adenoviruses, has allowed researchers to define the developmental origin of cardiac fibroblasts, elucidate their differentiation pathways, and functional mechanisms in cardiac injury and disease. In this review, we will first characterize the roles of fibroblasts in the different stages of cardiac repair and then examine novel techniques targeting fibroblasts post-ischemic heart injury. Full article
(This article belongs to the Special Issue Mechanisms of Ischemic Heart Injury)
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29 pages, 2226 KiB  
Review
Molecular Signaling to Preserve Mitochondrial Integrity against Ischemic Stress in the Heart: Rescue or Remove Mitochondria in Danger
by Justin D. Yu and Shigeki Miyamoto
Cells 2021, 10(12), 3330; https://doi.org/10.3390/cells10123330 - 27 Nov 2021
Cited by 11 | Viewed by 4166
Abstract
Cardiovascular diseases are one of the leading causes of death and global health problems worldwide, and ischemic heart disease is the most common cause of heart failure (HF). The heart is a high-energy demanding organ, and myocardial energy reserves are limited. Mitochondria are [...] Read more.
Cardiovascular diseases are one of the leading causes of death and global health problems worldwide, and ischemic heart disease is the most common cause of heart failure (HF). The heart is a high-energy demanding organ, and myocardial energy reserves are limited. Mitochondria are the powerhouses of the cell, but under stress conditions, they become damaged, release necrotic and apoptotic factors, and contribute to cell death. Loss of cardiomyocytes plays a significant role in ischemic heart disease. In response to stress, protective signaling pathways are activated to limit mitochondrial deterioration and protect the heart. To prevent mitochondrial death pathways, damaged mitochondria are removed by mitochondrial autophagy (mitophagy). Mitochondrial quality control mediated by mitophagy is functionally linked to mitochondrial dynamics. This review provides a current understanding of the signaling mechanisms by which the integrity of mitochondria is preserved in the heart against ischemic stress. Full article
(This article belongs to the Special Issue Mechanisms of Ischemic Heart Injury)
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17 pages, 764 KiB  
Review
Dynamic Regulation of Cysteine Oxidation and Phosphorylation in Myocardial Ischemia–Reperfusion Injury
by Kevin M. Casin and John W. Calvert
Cells 2021, 10(9), 2388; https://doi.org/10.3390/cells10092388 - 11 Sep 2021
Cited by 14 | Viewed by 3464
Abstract
Myocardial ischemia–reperfusion (I/R) injury significantly alters heart function following infarct and increases the risk of heart failure. Many studies have sought to preserve irreplaceable myocardium, termed cardioprotection, but few, if any, treatments have yielded a substantial reduction in clinical I/R injury. More research [...] Read more.
Myocardial ischemia–reperfusion (I/R) injury significantly alters heart function following infarct and increases the risk of heart failure. Many studies have sought to preserve irreplaceable myocardium, termed cardioprotection, but few, if any, treatments have yielded a substantial reduction in clinical I/R injury. More research is needed to fully understand the molecular pathways that govern cardioprotection. Redox mechanisms, specifically cysteine oxidations, are acute and key regulators of molecular signaling cascades mediated by kinases. Here, we review the role of reactive oxygen species in modifying cysteine residues and how these modifications affect kinase function to impact cardioprotection. This exciting area of research may provide novel insight into mechanisms and likely lead to new treatments for I/R injury. Full article
(This article belongs to the Special Issue Mechanisms of Ischemic Heart Injury)
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