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Molecular Diagnosis and Targeted Therapies in Ischemic Stroke
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Molecular Diagnosis and Targeted Therapies in Ischemic Stroke

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 March 2026 | Viewed by 2339

Special Issue Editors

Dr. Alicia Aliena-Valero

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Guest Editor
Instituto de Investigación Sanitaria La Fe, Valencia, Spain
Interests: ischemic stroke; cellular senescence; ageing; cerebroprotection
Dr. María Castelló-Ruiz

E-Mail Website
Guest Editor
Department of Cell Biology, Functional Biology and Physical Anthropology, Faculty of Biology, Universitat de València, Burjassot, 46100 Valencia, Spain
Interests: Ischaemic stroke; cellular senescence; cerebroprotection; oestrogens; ageing; inflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The field of ischemic stroke management has witnessed significant advances in recent years, with improved diagnostic tools and therapeutic options. However, the heterogeneity of ischemic stroke and the complex interplay of various factors continue to pose challenges in achieving optimal outcomes, and this remains a major global health challenge.

This Special Issue explores the multifaceted nature of ischemic stroke pathophysiology by integrating basic science research, translational studies, and clinical evidence. We aim to deepen our comprehension of the complex molecular mechanisms underlying ischemic stroke pathogenesis, such as oxidative stress, inflammation, and excitotoxicity. By identifying novel therapeutic targets, we can develop innovative treatments that address these mechanisms and potentially mitigate the damage caused by stroke. Furthermore, we seek to translate research findings into improved clinical practises for patients with ischemic stroke. These therapies may encompass neuroprotective agents, anti-inflammatory drugs, and strategies to enhance brain plasticity.

We invite submissions from researchers and professionals to share their latest findings and insights on this important topic.

Dr. Alicia Aliena-Valero
Dr. María Castelló-Ruiz
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 250 words) can be sent to the Editorial Office for assessment.

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • ischemic stroke
  • cerebral protection
  • repair treatments
  • therapeutic approaches

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Published Papers (3 papers)

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16 pages, 3820 KB  
Article
Complexity of Damage-Associated Molecular Pattern Molecule Expression Profile in Porcine Brain Affected by Ischemic Stroke
by Dominika Golubczyk, Aleksandra Mowinska, Piotr Holak, Piotr Walczak, Miroslaw Janowski and Izabela Malysz-Cymborska
Int. J. Mol. Sci. 2025, 26(8), 3702; https://doi.org/10.3390/ijms26083702 - 14 Apr 2025
Viewed by 1200
Abstract
Studies using large animal models are essential for better understanding the molecular processes underlying neurological diseases, including ischemic stroke, and serve as a robust foundation for evaluating potential therapies. To better understand the complex role of damage-associated molecular pattern molecules (DAMPs) after ischemia, [...] Read more.
Studies using large animal models are essential for better understanding the molecular processes underlying neurological diseases, including ischemic stroke, and serve as a robust foundation for evaluating potential therapies. To better understand the complex role of damage-associated molecular pattern molecules (DAMPs) after ischemia, we aimed to determine their expression in the porcine brain affected by ischemic stroke at four time points: 6 h, 24 h, 3 days and 7 days post-stroke. Within the first 24 h after the stroke, we observed the increased expression of several key factors, including calcium-binding proteins, peroxiredoxins, heat shock proteins and interleukins (1α and 1β, IL10, IL17α). Moreover, by day 7, multiple DAMPs were up-regulated, coinciding with an enhanced expression of vascular endothelial growth factor A (VEGFA) in the affected hemisphere. The effects of ischemic stroke were also evident systemically, as indicated by the altered serum levels of both pro- and anti-inflammatory interleukins, reflecting dynamic inflammatory response. To conclude, our findings provide new insights about the time-dependent DAMP activity in a large animal model of ischemic stroke, highlighting the simultaneous occurrence of an ongoing inflammatory response and the possible initiation of vascular remodeling as early as one week after stroke onset. Full article
(This article belongs to the Special Issue Molecular Diagnosis and Targeted Therapies in Ischemic Stroke)
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Review

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35 pages, 1095 KB  
Review
Cerebral Ischemia–Reperfusion Injury: Unraveling the Mitophagy–Oxidative Stress Axis for Neuroprotective Strategies
by Yanling Zhou, Baochun Luo, Tong Shang, Zengrong Wei and Wei Zou
Int. J. Mol. Sci. 2026, 27(5), 2448; https://doi.org/10.3390/ijms27052448 - 6 Mar 2026
Viewed by 147
Abstract
Cerebral ischemia–reperfusion (I/R) injury is a major pathological contributor to neurological deterioration following ischemic stroke (IS) and remains a critical barrier to effective neuroprotection. Accumulating evidence indicates that cerebral I/R injury is driven not by isolated stress responses but by coordinated and dynamic [...] Read more.
Cerebral ischemia–reperfusion (I/R) injury is a major pathological contributor to neurological deterioration following ischemic stroke (IS) and remains a critical barrier to effective neuroprotection. Accumulating evidence indicates that cerebral I/R injury is driven not by isolated stress responses but by coordinated and dynamic interactions among multiple cellular pathways. Among these, the bidirectional crosstalk between mitophagy and oxidative stress has emerged as a central regulatory axis. Moderate oxidative stress can function as an adaptive signal, activating protective mitophagy through key pathways such as AMPK/ULK1 signaling and cardiolipin externalization, thereby facilitating mitochondrial quality control and maintaining cellular homeostasis. Conversely, appropriately regulated mitophagy limits excessive reactive oxygen species (ROS) production by removing dysfunctional mitochondria, forming a negative feedback mechanism. However, dysregulation or excessive activation of either process disrupts this balance, leading to a self-amplifying cycle of mitochondrial dysfunction and oxidative damage that exacerbates neuronal injury. This review systematically summarizes the molecular mechanisms governing the oxidative stress–mitophagy crosstalk in cerebral I/R injury, highlighting key signaling nodes and regulatory pathways that determine protective versus detrimental outcomes. Furthermore, we discuss emerging therapeutic strategies aimed at precisely modulating this axis in a spatiotemporal- and intensity-dependent manner. By integrating mechanistic insights with translational perspectives, this review provides a conceptual framework for developing targeted neuroprotective interventions based on coordinated regulation of mitochondrial quality control and redox homeostasis. Full article
(This article belongs to the Special Issue Molecular Diagnosis and Targeted Therapies in Ischemic Stroke)
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28 pages, 1682 KB  
Review
Molecular Mechanisms and Targeted Intervention Strategies of Calcium Overload in Ischemic Stroke
by Yuwei Jiang, Guijun Wang, Shengming Jiang, Youjun Wang, Qi Tian and Mingchang Li
Int. J. Mol. Sci. 2026, 27(5), 2279; https://doi.org/10.3390/ijms27052279 - 28 Feb 2026
Viewed by 180
Abstract
Ischemic stroke is a leading cause of global neurological mortality and disability, characterized by a complex pathogenesis wherein calcium overload constitutes a pivotal mechanism in neuronal and glial cell death. Following ischemia and reperfusion, excitotoxicity triggered by excessive glutamate release activates NMDA receptors [...] Read more.
Ischemic stroke is a leading cause of global neurological mortality and disability, characterized by a complex pathogenesis wherein calcium overload constitutes a pivotal mechanism in neuronal and glial cell death. Following ischemia and reperfusion, excitotoxicity triggered by excessive glutamate release activates NMDA receptors and voltage-dependent calcium channels, leading to a large accumulation of intracellular Ca2+. This calcium dyshomeostasis subsequently initiates a cascade of detrimental events, including mitochondrial dysfunction, endoplasmic reticulum stress, reactive oxygen species generation, and the activation of calcium-dependent enzymes (such as calpain and phospholipase A2), ultimately culminating in cellular apoptosis or necrosis. In addition, calcium signaling imbalance is closely related to various forms of programmed cell death, such as ferroptosis and necroptosis. Research on calcium overload extends beyond neurons, with investigations in microglia and astrocytes yielding significant mechanistic insights. Although targeted interventions, encompassing calcium channel blockers, NMDA receptor antagonists, mitochondrial calcium homeostasis regulators, and calmodulin/calmodulin kinase (CaM/CaMK) inhibitors, have demonstrated preclinical progress, their clinical translation remains constrained. Future investigations should prioritize elucidating the nuanced regulatory mechanisms of calcium signaling pathways, developing highly selective and low-toxicity calcium intervention drugs, and combining multi-target treatment strategies such as neuroprotection, anti-inflammation, and tissue repair to provide theoretical basis and new solutions for the precise treatment of ischemic stroke. Full article
(This article belongs to the Special Issue Molecular Diagnosis and Targeted Therapies in Ischemic Stroke)
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