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Cells
Special Issues
Mechanisms Underlying Myocardial Ischemia/Reperfusion Injury and Cardioprotective Strategies
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Mechanisms Underlying Myocardial Ischemia/Reperfusion Injury and Cardioprotective Strategies

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 (30 June 2024) | Viewed by 1501

Special Issue Editors

Prof. Dr. Jianjie Ma

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Guest Editor
Department of Surgery, University of Virginia, Charlottesville, VA 22903, USA
Interests: regenerative medicine; cardiovascular diseases; aging; cancer biology; diabetes
Dr. Ki Ho Park

E-Mail
Guest Editor
Division of Surgical Sciences, Department of Surgery, University of Virginia, Charlottesville, VA 22903, USA
Interests: muscle physiology; ion channels; protein therapeutics; regenerative medicine

Special Issue Information

Dear Colleagues,

In patients who suffer myocardial infarction due to an initial heart attack, post-myocardial infarction oxidative stress and inflammation can cause continuous injury to cardiomyocytes, leading to heart failure. Effective therapeutic approaches that enhance cardiomyocyte integrity and mitigate inflammation are urgently needed for the critical care of post-myocardial infarction patients. Current advances in stem cell biology, nano-drug delivery, and precision medicine have paved the way for innovative approaches to treat acute myocardial infarction and the transition to heart failure.

This Special Issue will examine the cellular and molecular bases that underlie the protection of myocardial integrity and control of inflammation that contribute to the regenerative process of the heart under stress, aging or infectious conditions. Engineering/delivery of stem cells, CRISPR-gene editing or AAV-gene delivery that can boost the regenerative process of the heart are of great interest for this Special Issue.

Prof. Dr. Jianjie Ma
Dr. Ki Ho Park
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. 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

  • myocardial infarction
  • heart failure
  • stem cells
  • nanoparticle
  • aging
  • diabetes
  • transplantation
  • CRISPR
  • AAV
  • tissue repair
  • inflammation
  • NETosis
  • pyroptosis
  • mitochondria

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Published Papers (2 papers)

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Research

14 pages, 7299 KiB  
Article
Novel Fluorescence-Based Methods to Determine Infarct and Scar Size in Murine Models of Reperfused Myocardial Infarction
by Ashley Duplessis, Christin Elster, Stefanie Becher, Christina Engel, Alexander Lang, Madlen Kaldirim, Christian Jung, Maria Grandoch, Malte Kelm, Susanne Pfeiler and Norbert Gerdes
Cells 2024, 13(19), 1633; https://doi.org/10.3390/cells13191633 - 30 Sep 2024
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Abstract
Determination of infarct and scar size following myocardial infarction (MI) is commonly used to evaluate the efficacy of potential cardioprotective treatments in animal models. However, histological methods to determine morphological features in the infarcted heart have barely improved since implementation while still consuming [...] Read more.
Determination of infarct and scar size following myocardial infarction (MI) is commonly used to evaluate the efficacy of potential cardioprotective treatments in animal models. However, histological methods to determine morphological features in the infarcted heart have barely improved since implementation while still consuming large parts of the tissue and offering little options for parallel analyses. We aim to develop a new fluorescence technology for determining infarct area and area at risk that is comparable to 2,3,5-triphenyltetrazolium chloride (TTC) staining but allows for multiple analyses on the same heart tissue. For early and late time points following MI, we compared classical histochemical approaches with fluorescence staining methods. Reperfused MI was induced in male mice, the hearts were extracted 24 h, 7-, 21-, or 28-days later and fluorescently stained by combining Hoechst and phalloidin. This approach allowed for clear visualization of the infarct area, the area at ischemic risk and the remote area not affected by MI. The combined fluorescence staining correlated with the classic TTC/Evans Blue staining 24 h after MI (r = 0.8334). In later phases (>7 d) post-MI, wheat germ agglutinin (WGA) is equally accurate as classical Sirius Red (r = 0.9752), Masson’s (r = 0.9920) and Gomori’s Trichrome (r = 0.8082) staining for determination of scar size. Additionally, feasibility to co-localize fluorescence-stained immune cells in specific regions of the infarcted myocardium was demonstrated with this protocol. In conclusion, this new procedure for determination of post-MI infarct size is not inferior to classical TTC staining, yet provides substantial benefits, including the option for unbiased software-assisted analysis while sparing ample residual tissue for additional analyses. Overall, this enhances the data quality and reduces the required animal numbers consistent with the 3R concept of animal experimentation. Full article
(This article belongs to the Special Issue Mechanisms Underlying Myocardial Ischemia/Reperfusion Injury and Cardioprotective Strategies)
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17 pages, 12316 KiB  
Article
Roxadustat Attenuates Adverse Remodeling Following Myocardial Infarction in Mice
by Marc-Michael Zaruba, Simon Staggl, Santhosh Kumar Ghadge, Thomas Maurer, Jasmina Gavranovic-Novakovic, Vivek Jeyakumar, Patric Schönherr, Andreas Wimmer, Gerhard Pölzl, Axel Bauer and Moritz Messner
Cells 2024, 13(13), 1074; https://doi.org/10.3390/cells13131074 - 21 Jun 2024
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Abstract
Activation of the CXCL12/CXCR4/ACKR3 axis is known to aid myocardial repair through ischemia-triggered hypoxia-inducible factor-1α (HIF-1α). To enhance the upregulation of HIF-1α, we administered roxadustat, a novel prolyl hydroxylase inhibitor (PHI) clinically approved by the European Medicines Agency 2021 for the treatment of [...] Read more.
Activation of the CXCL12/CXCR4/ACKR3 axis is known to aid myocardial repair through ischemia-triggered hypoxia-inducible factor-1α (HIF-1α). To enhance the upregulation of HIF-1α, we administered roxadustat, a novel prolyl hydroxylase inhibitor (PHI) clinically approved by the European Medicines Agency 2021 for the treatment of renal anemia, with the purpose of improving LV function and attenuating ischemic cardiomyopathy. Methods: We evaluated roxadustat’s impact on HIF-1 stimulation, cardiac remodeling, and function after MI. Therefore, we analyzed nuclear HIF-1 expression, the mRNA and protein expression of key HIF-1 target genes (RT-PCR, Western blot), inflammatory cell infiltration (immunohistochemistry), and apoptosis (TUNEL staining) 7 days after MI. Additionally, we performed echocardiography in male and female C57BL/6 mice 28 days post-MI. Results: We found a substantial increase in nuclear HIF-1, associated with an upregulation of HIF-1α target genes like CXCL12/CXCR4/ACKR3 at the mRNA and protein levels. Roxadustat increased the proportion of myocardial reparative M2 CD206+ cells, suggesting beneficial alterations in immune cell migration and a trend towards reduced apoptosis. Echocardiography showed that roxadustat treatment significantly preserved ejection fraction and attenuated subsequent ventricular dilatation, thereby reducing adverse remodeling. Conclusions: Our findings suggest that roxadustat is a promising clinically approved treatment option to preserve myocardial function by attenuating adverse remodeling. Full article
(This article belongs to the Special Issue Mechanisms Underlying Myocardial Ischemia/Reperfusion Injury and Cardioprotective Strategies)
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