Submit to Special Issue Submit Abstract to Special Issue Review for CIMB Propose a Special Issue

Journal Menu

Journal Browser

Molecular Mechanisms and Treatment of Ischemia–Reperfusion Injury

Special Issue Editors
Special Issue Information
Keywords
Benefits of Publishing in a Special Issue
Published Papers

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 30 September 2024 | Viewed by 2897

Share This Special Issue

Special Issue Editor

Prof. Dr. Jun Kobayashi

E-Mail Website
Guest Editor

Department of Clinical Dietetics and Human Nutrition, Faculty of Pharmaceutical Science, Josai University, 1-1 Keyakidai, Sakado 350-0295, Japan
Interests: nitric oxide; nitrate/nitrite; crush syndrome; ischemia/reperfusion injury; reactive oxygen species
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Ischemia–reperfusion (I/R) injury is caused by a temporary restriction of blood supply to a particular organ, such as the heart, brain, kidney, liver and skeletal muscle. Subsequent reperfusion to these hypoxic or anoxic organs causes organ dysfunction and tissue cell death, sometimes leading to systemic circulatory shock. Although the organ type, as well as magnitude and duration of the interruption in the blood supply are critical determinants of whether the organ becomes necrotic or not, organ damage is essentially caused by oxidative stress following reperfusion, which induces cell membrane lipid peroxidation, mitochondrial dysfunction and subsequent inflammatory responses, such as neutrophil activation and the release of reactive oxygen species and other inflammatory mediators, including adhesion molecules and various cytokines. Effective pharmacological agents and methods to combat I/R injury have recently been developed. Nevertheless, we are far from establishing the treatment for this disease. I, therefore, look forward to fruitful discussions on this theme, particularly from the standpoint of molecular biology, and call for original articles and reviews focusing on the pathophysiology of I/R injury, development of animal models, and development of new pharmacological and interventional strategies. This Special Issue will provide a key resource to the readers of CIMB, including new findings related to I/R injury with the potential to lead to novel treatment strategies.

Prof. Dr. Jun Kobayashi
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. Current Issues in Molecular Biology 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 2200 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
myocardial infarction
cerebral infarction
renal infarction
crush syndrome
oxidative stress
reactive oxygen species

Benefits of Publishing in a Special Issue

Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (4 papers)

Download All Papers

Order results

Result details

Show export options Show export options

Select all

Export citation of selected articles as:

Research

11 pages, 1993 KiB

Open AccessArticle

The Role of Mannitol and Vitamin D in Ovarian Ischemia/Reperfusion Injury in Rats with Acute Abdominal

by Faruk Karateke, Atilla Karateke, Basak Topdagi, Merve Atilgan and Recep Dokuyucu

Curr. Issues Mol. Biol. 2024, 46(8), 8903-8913; https://doi.org/10.3390/cimb46080526 - 15 Aug 2024

Viewed by 743

Abstract

This study was designed to investigate the effects of vitamin D and mannitol in an experimental rat ovarian torsion model. Thirty-two female Wistar albino rats were randomly classified as group 1: (sham), group 2: (detorsion), group 3: (detorsion + mannitol), group 4: (detorsion + vitamin D) and group 5: (detorsion + mannitol + vitamin D) (for each group n = 8). All groups were subjected to bilateral adnexal torsion for 2 h except for group 1. Bilateral adnexal detorsion was performed in all groups except for group 1. Groups 3 and 5 intraperitoneally received the injection of mannitol at a dose of 0.3 mg/kg 30 min before detorsion. Also, the group’s 4 and 5 orally received vitamin D in a dose of 500 IU/kg/day for two weeks before torsion. Total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI) and proliferating cell nuclear antigen (PCNA) levels were analyzed. According to the histopathological analyses, ovarian tissue damage and follicle counting were evaluated. TOS, OSI and histopathologic score values of ovarian tissue were significantly lower in group 5 than groups 2, 3 and 4 (p < 0.05). The PCNA level was significantly higher in group 5 than in groups 2, 3 and 4 (p < 0.05). A strong negative correlation was found between OSI and PCNA in groups 2, 3, 4 and 5 (r = −0.92, p = 0.01; r = −0.98, p < 0.0001; r = −0.98, p < 0.0001 and r = −0.96, p = 0.0002, respectively). The numbers of primordial follicles in group 5 (p < 0.001) and primary follicles in group 4 (p < 0.001) were significantly higher when compared to group 2. Based on the results of this study, it could be suggested that combination treatment of mannitol with vitamin D is more effective in reversing tissue damage induced by ischemia–reperfusion (I/R) injury in the ovarian torsion model than administration of only an agent. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Treatment of Ischemia–Reperfusion Injury)

► Show Figures

Figure 1

16 pages, 6733 KiB

Open AccessArticle

The Combined Delivery of the Vegf, Ang, and Gdnf Genes Stimulates Angiogenesis and Improves Post-Ischemic Innervation and Regeneration in Skeletal Muscle

by Igor Valerievich Samatoshenkov, Alexander Maazovich Aimaletdinov, Elena Yurievna Zakirova, Yuri Alexandrovich Chelyshev, Julia Maratovna Samatoshenkova, Marat Salimovich Kadyrov, Evgeny Alekseevich Kniazev, Bulat Ilgamovich Salakhov and Yana Olegovna Mukhamedshina

Curr. Issues Mol. Biol. 2024, 46(8), 8611-8626; https://doi.org/10.3390/cimb46080507 - 5 Aug 2024

Viewed by 586

Abstract

In this study, the effects of different combinations of the genes Vegf, Ang, and Gdnf injected both using direct virus-mediated injection (adenovirus, Ad5) and umbilical cord blood mononuclear cells (UCBCs) on the processes of stimulation of post-ischemic innervation, angiogenesis, and regeneration in skeletal muscle were investigated in a rat hindlimb chronic ischemia model. It was shown that more pronounced stimulation of angiogenesis and restoration of post-ischemic innervation were achieved both in the early (28 days post-ischemia, dpi) and late (42 dpi) terms of the experiment in the calf muscle when UCBCs delivered the combination of Ad5-Vegf and Ad5-Ang compared to the direct injection of the same vector combination into the area of ischemia. At the same time, the inclusion of Ad5-Gdnf in the combination of Ad5-Vegf and Ad5-Ang directly injected or administered by UCBCs provided a significant increase in the number of centronuclear muscle fibers, indicating stimulation of post-ischemic reparative myogenesis. This study allowed us to determine the most effective gene combinations for angiogenesis and neurogenesis, which, in the future, may serve as the basis for the development of gene and gene cell products for the treatment of chronic lower limb ischemia. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Treatment of Ischemia–Reperfusion Injury)

► Show Figures

Graphical abstract

13 pages, 11373 KiB

Open AccessArticle

Skimmianine Showed Neuroprotection against Cerebral Ischemia/Reperfusion Injury

by Hayat Ayaz, Fırat Aşır and Tuğcan Korak

Curr. Issues Mol. Biol. 2024, 46(7), 7373-7385; https://doi.org/10.3390/cimb46070437 - 12 Jul 2024

Viewed by 540

Abstract

The aim of this study was to investigate the antioxidant and anti-inflammatory effects of skimmianine on cerebral ischemia–reperfusion (IR) injury. Twenty-four female Wistar albino rats were randomly divided into three groups: Sham, Ischemia–Reperfusion (IR), and IR + Skimmianine (40 mg/kg Skimmianine). Cerebral ischemia was induced using a monofilament nylon suture to occlude the middle cerebral artery for 60 min. Following 23 h of reperfusion, the animals were sacrificed 14 days later. The effects of skimmianine on brain tissue post-IR injury were examined through biochemical and immunochemical analyses. In silico analysis using the Enrichr platform explored skimmianine’s potential biological processes involving IBA-1, IL-6, and NF-κB proteins. In the IR group, MDA levels increased, while SOD and CAT antioxidant enzyme activities decreased. In the IR + Skimmianine group, skimmianine treatment resulted in decreased MDA levels and increased SOD and CAT activities. Significant increases in IBA-1 expression were observed in the IR group, which skimmianine treatment significantly reduced, modulating microglial activation. High levels of IL-6 expression were noted in pyramidal neurons, vascular structures, and neuroglial cells in the IR group; skimmianine treatment reduced IL-6 expression, demonstrating anti-inflammatory effects. Increased NF-κB expression was observed in neurons and blood vessels in the gray and white matter in the IR group; skimmianine treatment reduced NF-κB expression. Gene Ontology results suggest skimmianine impacts immune and inflammatory responses via IBA-1 and IL-6, with potential effects on estrogen mechanisms mediated by NF-κB. Skimmianine may be a potential therapeutic strategy due to its antioxidant and anti-inflammatory effects on cerebral IR injury. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Treatment of Ischemia–Reperfusion Injury)

► Show Figures

Figure 1

20 pages, 2641 KiB

Open AccessArticle

The Autophagic and Apoptotic Death of Forebrain Neurons of Rats with Global Brain Ischemia Is Diminished by the Intranasal Administration of Insulin: Possible Mechanism of Its Action

by Irina O. Zakharova, Liubov V. Bayunova, Daria K. Avrova, Alina D. Tretyakova, Alexander O. Shpakov and Natalia F. Avrova

Curr. Issues Mol. Biol. 2024, 46(7), 6580-6599; https://doi.org/10.3390/cimb46070392 - 27 Jun 2024

Viewed by 485

Abstract

Insulin is a promising neuroprotector. To better understand the mechanism of insulin action, it was important to show its ability to diminish autophagic neuronal death in animals with brain ischemic and reperfusion injury. In forebrain ischemia and reperfusion, the number of live neurons in the hippocampal CA1 region and frontal cortex of rats decreased to a large extent. Intracerebroventricular administration of the autophagy and apoptosis inhibitors to ischemic rats significantly increased the number of live neurons and showed that the main part of neurons died from autophagy and apoptosis. Intranasal administration of 0.5 IU of insulin per rat (before ischemia and daily during reperfusion) increased the number of live neurons in the hippocampal CA1 region and frontal brain cortex. In addition, insulin significantly diminished the level of autophagic marker LC3B-II in these forebrain regions, which markedly increased during ischemia and reperfusion. Our studies demonstrated for the first time the ability of insulin to decrease autophagic neuronal death, caused by brain ischemia and reperfusion. Insulin administered intranasally activated the Akt-kinase (activating the mTORC1 complex, which inhibits autophagy) and inhibited the AMP-activated protein kinase (which activates autophagy) in the hippocampus and frontal cortex of rats with brain ischemia and reperfusion. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Treatment of Ischemia–Reperfusion Injury)

► Show Figures

Journal Menu

Journal Browser

Molecular Mechanisms and Treatment of Ischemia–Reperfusion Injury

Share This Special Issue

Special Issue Editor

Special Issue Information

Keywords

Benefits of Publishing in a Special Issue

Published Papers (4 papers)

Research

Further Information

Guidelines

MDPI Initiatives

Follow MDPI