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Cells
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Myocardial Ischemia/Reperfusion Injury: Mechanisms and New Directions in Cardioprotection
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Myocardial Ischemia/Reperfusion Injury: Mechanisms and New Directions in Cardioprotection

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Tissues and Organs".

Deadline for manuscript submissions: 30 November 2025 | Viewed by 1308

Special Issue Editor

Dr. Sauri Hernandez-Resendiz

E-Mail Website
Guest Editor
Cardiovascular and Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore 8 College Road, Singapore 169857, Singapore
Interests: myocardial infarction; heart failure; cardiac metabolism; mitochondria; cardioprotection
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

I am pleased to invite contributions that address one of the most urgent challenges in cardiovascular medicine: preventing heart failure following acute myocardial infarction (AMI). Despite advances in pharmacological therapies and interventional cardiology, heart failure remains a leading cause of long-term morbidity and mortality among AMI survivors. A major contributor to this outcome is ischemia–reperfusion (I/R) injury, an event that paradoxically exacerbates heart damage when blood flow is restored.

This Special Issue aims to spotlight recent breakthroughs in understanding the cellular and molecular mechanisms driving I/R injury and heart failure, focusing on mitochondria, inflammation, and metabolic remodeling. We aim to showcase innovative therapeutic strategies that have the potential to move from bench to bedside and ultimately improve patient outcomes.

We welcome original research articles, comprehensive reviews, expert perspectives investigating cellular mechanisms of I/R injury, novel molecular targets, innovative therapeutic strategies, and translational approaches in the context of myocardial infarction and heart failure.

Suggested topics include but are not limited to the following:

  1. Mitochondrial dynamics and cardioprotection;
  2. New insights into inflammation and oxidative stress in I/R injury;
  3. Emerging small molecules and peptides for cardioprotection;
  4. Cell-based therapies and regenerative medicine in AMI;
  5. Exosomes and extracellular vesicles therapies;
  6. Nanomedicine and targeted drug delivery in cardiovascular therapy;
  7. Artificial intelligence and applications in I/R research.

Dr. Sauri Hernandez-Resendiz
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

  • myocardial infarction
  • heart failure
  • ischemia/reperfusion injury
  • no-reflow phenomenon
  • oxidative stress
  • cell death
  • cardiac metabolism
  • mitochondrial quality control
  • inflammation
  • cardioprotection

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Published Papers (2 papers)

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Review

33 pages, 4216 KB  
Review
Myocardial Ischemia/Reperfusion Injury: Molecular Insights, Forensic Perspectives, and Therapeutic Horizons
by Maria Sofia Fede, Gloria Daziani, Francesco Tavoletta, Angelo Montana, Paolo Compagnucci, Gaia Goteri, Margherita Neri and Francesco Paolo Busardò
Cells 2025, 14(19), 1509; https://doi.org/10.3390/cells14191509 - 27 Sep 2025
Viewed by 561
Abstract
Acute myocardial infarction (AMI) remains the leading cause of death worldwide, with myocardial ischemia/reperfusion injury (MIRI) emerging as a significant factor influencing patient outcomes despite timely reperfusion therapy. MIRI refers to paradoxical myocardial damage that occurs upon restoration of coronary blood flow and [...] Read more.
Acute myocardial infarction (AMI) remains the leading cause of death worldwide, with myocardial ischemia/reperfusion injury (MIRI) emerging as a significant factor influencing patient outcomes despite timely reperfusion therapy. MIRI refers to paradoxical myocardial damage that occurs upon restoration of coronary blood flow and is driven by complex inflammatory, oxidative, and metabolic mechanisms, which can exacerbate infarct size (IS), contributing to adverse outcomes. This review explores the molecular and cellular pathophysiology of MIRI, emphasizing both its clinical and forensic relevance. The principal mechanisms discussed include oxidative stress and mitochondrial dysfunction, calcium overload and ion homeostasis imbalance, inflammatory responses, with particular focus on the NLRP3 inflammasome and cytokine pathways, and multiple forms of cell death (apoptosis, necroptosis, pyroptosis, and autophagy). Additionally, the authors present original immunohistochemical findings from autopsy cases of patients who suffered ST-segment elevation myocardial infarction (STEMI) and underwent percutaneous coronary intervention (PCI), but subsequently died. These findings underscore that successful reperfusion does not completely prevent delayed complications, like arrhythmias, ventricular fibrillation (VF), and sudden cardiac death (SCD), often caused by secondary MIRI-related mechanisms. Moreover, the case series highlight the diagnostic value of inflammatory markers for pathologists in identifying MIRI as a contributing factor in such fatalities. Finally, immunotherapeutic strategies—including IL-1 and IL-6 inhibitors such as Canakinumab and Tocilizumab—are reviewed for their potential to reduce cardiovascular events and mitigate the effects of MIRI. The review advocates for continued multidisciplinary research aimed at improving our understanding of MIRI, developing effective treatments, and informing forensic investigations of reperfusion-related deaths. Full article
(This article belongs to the Special Issue Myocardial Ischemia/Reperfusion Injury: Mechanisms and New Directions in Cardioprotection)
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Graphical abstract

18 pages, 1677 KB  
Review
The Cytoskeletal Structure in Cardiomyocyte Maturation and Proliferation
by Aldana Rojas, Shelby Dahlen, Feng Zhang and Shijie Liu
Cells 2025, 14(19), 1494; https://doi.org/10.3390/cells14191494 - 24 Sep 2025
Viewed by 523
Abstract
The adult heart has a limited ability to regenerate, which is partly due to the structural and metabolic specialization that cardiomyocytes (CMs) acquire during postnatal maturation. In this review, we explore how cytoskeletal remodeling, metabolic reprogramming, and interactions with the extracellular matrix (ECM) [...] Read more.
The adult heart has a limited ability to regenerate, which is partly due to the structural and metabolic specialization that cardiomyocytes (CMs) acquire during postnatal maturation. In this review, we explore how cytoskeletal remodeling, metabolic reprogramming, and interactions with the extracellular matrix (ECM) regulate CM maturation, proliferation, and the potential for regeneration. We describe how the assembly of microtubules, actin filaments, and sarcomeric structures is essential for developing contractile function, but also creates structural barriers that prevent cell division. Recent studies show that disassembling these cytoskeletal components, along with activating signaling pathways such as Hippo-YAP, Wnt, and NRG1/ErbB4, can promote CM dedifferentiation and re-entry into the cell cycle. Metabolic shifts also play a critical role. A return from oxidative phosphorylation to glycolysis also leads to CM dedifferentiation and proliferation. In addition, changes in ECM composition and mechanical signaling affect cytoskeletal dynamics and regenerative capacity. Understanding how these structural, metabolic, and signaling networks work together opens the door to new approaches for restoring heart function after injury. Full article
(This article belongs to the Special Issue Myocardial Ischemia/Reperfusion Injury: Mechanisms and New Directions in Cardioprotection)
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