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Biomedicines
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Molecular Mechanisms and Translational Aspects of Ischemia-Reperfusion Injury
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Molecular Mechanisms and Translational Aspects of Ischemia-Reperfusion Injury

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (31 August 2023) | Viewed by 9462

Special Issue Editors

Dr. Alexandra Gratl

E-Mail Website
Guest Editor
Department of Vascular Surgery, Medical University Innsbruck, Innsbruck, Austria
Interests: aortic aneurysm surgery; spinal cord ischemia; mitochondrial function; carotid artery disease; peripheral arterial disease
Prof. Dr. Sabine Helena Wipper

E-Mail Website
Guest Editor
Department of Vascular Surgery, Medical University Innsbruck, Innsbruck, Austria
Interests: aortic diseases; endovascular surgery; microperfusion; peripheral arterial disease; carotid arteries; vascular imaging
Special Issues, Collections and Topics in MDPI journals
Dr. Florian Enzmann

E-Mail Website
Guest Editor
Department of Vascular Surgery, Medical University Innsbruck, Innsbruck, Austria
Interests: peripheral arterial disease; bypass surgery; endovascular interventions
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Ischemia reperfusion injury (IRI) is a relevant pathophysiological mechanism in different fields of vascular surgery (e.g., IRI following acute limb ischemia and IRI of the spinal cord in aortic aneurysm therapy), but also affects other specialties such as solid organ transplantation and cardiothoracic surgery. Besides the clinical consequences of IRI on the outcome of patients, the molecular mechanisms involved in IRI have been the focus of numerous research projects in the past. Defining specific pathways involved in IRI (e.g., reactive oxygen species, free radicals, mitochondrial pathways) is essential to find new therapeutic targets and develop techniques to mitigate or prevent IRI.

In this Special Issue of Biomedicines, we invite you to contribute original research articles, reviews or commentaries on all aspects related to the theme of “Molecular Mechanisms and Translational Aspects of Ischemia-Reperfusion Injury”.

The aim of this Special Issue of Biomedicines is to cover and discuss all experimental, translational as well as clinical aspects of molecular mechanisms involved in the pathophysiology of IRI at biochemical, cellular, functional and translational levels.

Dr. Alexandra Gratl
Prof. Dr. Sabine Helena Wipper
Dr. Florian Enzmann
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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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

  • ischemia reperfusion injury
  • reactive oxygen species
  • free radicals
  • mitochondrial pathways

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Published Papers (4 papers)

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Research

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10 pages, 1197 KiB  
Article
Mitochondrial Creatine Kinase 2 (Ckmt2) as a Plasma-Based Biomarker for Evaluating Reperfusion Injury in Acute Myocardial Infarction
by Alexander Lang, Daniel Oehler, Marcel Benkhoff, Yvonne Reinders, Maike Barcik, Khatereh Shahrjerdi, Madlen Kaldirim, Albert Sickmann, Lisa Dannenberg, Amin Polzin, Susanne Pfeiler, Malte Kelm, Maria Grandoch, Christian Jung and Norbert Gerdes
Biomedicines 2024, 12(10), 2368; https://doi.org/10.3390/biomedicines12102368 - 16 Oct 2024
Viewed by 1541
Abstract
Background/Objectives: Acute myocardial infarction (AMI), characterized by irreversible heart muscle damage and impaired cardiac function caused by myocardial ischemia, is a leading cause of global mortality. The damage associated with reperfusion, particularly mitochondrial dysfunction and reactive oxygen species (ROS) formation, has emerged as [...] Read more.
Background/Objectives: Acute myocardial infarction (AMI), characterized by irreversible heart muscle damage and impaired cardiac function caused by myocardial ischemia, is a leading cause of global mortality. The damage associated with reperfusion, particularly mitochondrial dysfunction and reactive oxygen species (ROS) formation, has emerged as a crucial factor in the pathogenesis of cardiac diseases, leading to the recognition of mitochondrial proteins as potential markers for myocardial damage. This study aimed to identify differentially expressed proteins based on the type of cardiac injury, in particular those with and without reperfusion. Methods: Male C57Bl/6J mice were either left untreated, sham-operated, received non-reperfused AMI, or reperfused AMI. Twenty-four hours after the procedures, left ventricular (LV) function and morphological changes including infarct size were determined using echocardiography and triphenyl tetrazolium chloride (TTC) staining, respectively. In addition, plasma was isolated and subjected to untargeted mass spectrometry and, further on, the ELISA-based validation of candidate proteins. Results: We identified mitochondrial creatine kinase 2 (Ckmt2) as a differentially regulated protein in plasma of mice with reperfused but not non-reperfused AMI. Elevated levels of Ckmt2 were significantly associated with infarct size and impaired LV function following reperfused AMI, suggesting a specific involvement in reperfusion damage. Conclusions: Our study highlights the potential of plasma Ckmt2 as a biomarker for assessing reperfusion injury and its impact on cardiac function and morphology in the acute phase of MI. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Translational Aspects of Ischemia-Reperfusion Injury)
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18 pages, 4405 KiB  
Article
NLRP3-Inflammasome Inhibition with IZD334 Does Not Reduce Cardiac Damage in a Pig Model of Myocardial Infarction
by Max J. M. Silvis, Evelyne J. Demkes, Leo Timmers, Fatih Arslan, Saskia C. A. de Jager, Joost P. G. Sluijter, Arend Mosterd, Dominique P. V. de Kleijn, Lena Bosch and Gerardus P. J. van Hout
Biomedicines 2022, 10(12), 3056; https://doi.org/10.3390/biomedicines10123056 - 28 Nov 2022
Cited by 6 | Viewed by 2559
Abstract
NLRP3-inflammasome-mediated signaling is thought to significantly contribute to the extent of myocardial damage after myocardial infarction (MI). The purpose of this study was to investigate the effects of the NLRP3-inflammasome inhibitor IZD334 on cardiac damage in a pig model of myocardial infarction. Prior [...] Read more.
NLRP3-inflammasome-mediated signaling is thought to significantly contribute to the extent of myocardial damage after myocardial infarction (MI). The purpose of this study was to investigate the effects of the NLRP3-inflammasome inhibitor IZD334 on cardiac damage in a pig model of myocardial infarction. Prior to in vivo testing, in vitro, porcine peripheral blood mononuclear cells and whole blood were treated with increasing dosages of IZD334, a novel NLRP3-inflammasome inhibitor, and were stimulated with lipopolysaccharide (LPS) and adenosine triphosphate (ATP). After determination of the pharmacological profile in healthy pigs, thirty female Landrace pigs were subjected to 75 min of transluminal balloon occlusion of the LAD coronary artery and treated with placebo or IZD334 (1 mg/kg, 3 mg/kg, or 10 mg/kg once daily) in a blinded randomized fashion. In vitro, NLRP3-inflammasome stimulation showed the pronounced release of interleukin (IL)-1β that was attenuated by IZD334 (p < 0.001). In vivo, no differences were observed between groups in serological markers of inflammation nor myocardial IL-1β expression. After 7 days, the ejection fraction did not differ between groups, as assessed with MRI (placebo: 45.1 ± 8.7%, 1 mg/kg: 49.9 ± 6.1%, 3 mg/kg: 42.7 ± 3.8%, 10 mg/kg: 44.9 ± 6.4%, p = 0.26). Infarct size as a percentage of the area at risk was not reduced (placebo: 73.1 ± 3.0%, 1 mg/kg: 75.5 ± 7.3%, 3 mg/kg: 80.3 ± 3.9%, 10 mg/kg: 78.2 ± 8.0%, p = 0.21). In this pig MI model, we did not observe attenuation of the inflammatory response after NLRP3-inflammasome inhibition in vivo. Consecutively, no difference was observed in IS and cardiac function, while in vitro inhibition successfully reduced IL-1β release from stimulated porcine blood cells. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Translational Aspects of Ischemia-Reperfusion Injury)
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16 pages, 2996 KiB  
Article
Neuroprotective Effects of the Lithium Salt of a Novel JNK Inhibitor in an Animal Model of Cerebral Ischemia–Reperfusion
by Igor A. Schepetkin, Galina A. Chernysheva, Oleg I. Aliev, Liliya N. Kirpotina, Vera I. Smol’yakova, Anton N. Osipenko, Mark B. Plotnikov, Anastasia R. Kovrizhina, Andrei I. Khlebnikov, Evgenii V. Plotnikov and Mark T. Quinn
Biomedicines 2022, 10(9), 2119; https://doi.org/10.3390/biomedicines10092119 - 29 Aug 2022
Cited by 10 | Viewed by 2471
Abstract
The c-Jun N-terminal kinases (JNKs) regulate many physiological processes, including inflammatory responses, morphogenesis, cell proliferation, differentiation, survival, and cell death. Therefore, JNKs represent attractive targets for therapeutic intervention. In an effort to develop improved JNK inhibitors, we synthesized the lithium salt of [...] Read more.
The c-Jun N-terminal kinases (JNKs) regulate many physiological processes, including inflammatory responses, morphogenesis, cell proliferation, differentiation, survival, and cell death. Therefore, JNKs represent attractive targets for therapeutic intervention. In an effort to develop improved JNK inhibitors, we synthesized the lithium salt of 11H-indeno[1,2-b]quinoxaline-11-one oxime (IQ-1L) and evaluated its affinity for JNK and biological activity in vitro and in vivo. According to density functional theory (DFT) modeling, the Li+ ion stabilizes the six-membered ring with the 11H-indeno[1,2-b]quinoxaline-11-one (IQ-1) oximate better than Na+. Molecular docking showed that the Z isomer of the IQ-1 oximate should bind JNK1 and JNK3 better than (E)-IQ-1. Indeed, experimental analysis showed that IQ-1L exhibited higher JNK1-3 binding affinity in comparison with IQ-1S. IQ-1L also was a more effective inhibitor of lipopolysaccharide (LPS)-induced nuclear factor-κB/activating protein 1 (NF-κB/AP-1) transcriptional activity in THP-1Blue monocytes and was a potent inhibitor of proinflammatory cytokine production by MonoMac-6 monocytic cells. In addition, IQ-1L inhibited LPS-induced c-Jun phosphorylation in MonoMac-6 cells, directly confirming JNK inhibition. In a rat model of focal cerebral ischemia (FCI), intraperitoneal injections of 12 mg/kg IQ-1L led to significant neuroprotective effects, decreasing total neurological deficit scores by 28, 29, and 32% at 4, 24, and 48 h after FCI, respectively, and reducing infarct size by 52% at 48 h after FCI. The therapeutic efficacy of 12 mg/kg IQ-1L was comparable to that observed with 25 mg/kg of IQ-1S, indicating that complexation with Li+ improved efficacy of this compound. We conclude that IQ-1L is more effective than IQ-1S in treating cerebral ischemia injury and thus represents a promising anti-inflammatory compound. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Translational Aspects of Ischemia-Reperfusion Injury)
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Review

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14 pages, 584 KiB  
Review
Biomarkers of Spinal Cord Injury in Patients Undergoing Complex Endovascular Aortic Repair Procedures—A Narrative Review of Current Literature
by Anna Sotir, Johannes Klopf, Christine Brostjan, Christoph Neumayer and Wolf Eilenberg
Biomedicines 2023, 11(5), 1317; https://doi.org/10.3390/biomedicines11051317 - 28 Apr 2023
Cited by 2 | Viewed by 2003
Abstract
Complex endovascular aortic repair (coEVAR) of thoracoabdominal aortic aneurysms (TAAA) has greatly evolved in the past decades. Despite substantial improvements of postoperative care, spinal cord injury (SCI) remains the most devastating complication of coEVAR being associated with impaired patient outcome and having an [...] Read more.
Complex endovascular aortic repair (coEVAR) of thoracoabdominal aortic aneurysms (TAAA) has greatly evolved in the past decades. Despite substantial improvements of postoperative care, spinal cord injury (SCI) remains the most devastating complication of coEVAR being associated with impaired patient outcome and having an impact on long-term survival. The rising number of challenges of coEVAR, essentially associated with an extensive coverage of critical blood vessels supplying the spinal cord, resulted in the implementation of dedicated SCI prevention protocols. In addition to maintenance of adequate spinal cord perfusion pressure (SCPP), early detection of SCI plays an integral role in intra- and postoperative patient care. However, this is challenging due to difficulties with clinical neurological examinations during patient sedation in the postoperative setting. There is a rising amount of evidence, suggesting that subclinical forms of SCI might be accompanied by an elevation of biochemical markers, specific to neuronal tissue damage. Addressing this hypothesis, several studies have attempted to assess the potential of selected biomarkers with regard to early SCI diagnosis. In this review, we discuss biomarkers measured in patients undergoing coEVAR. Once validated in future prospective clinical studies, biomarkers of neuronal tissue damage may potentially add to the armamentarium of modalities for early SCI diagnosis and risk stratification. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Translational Aspects of Ischemia-Reperfusion Injury)
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