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Cells
Special Issues
Molecular and Cellular Mechanisms of Ischemic Stroke
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Molecular and Cellular Mechanisms of Ischemic Stroke

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 31 August 2026 | Viewed by 975

Editor

Dr. Milani Deb-Chatterji

E-Mail Website
Guest Editor
Department of Neurology, University Medical Center Schleswig-Holstein, Campus Kiel, 24105 Kiel, Germany
Interests: ischemic stroke; vasculitis; acute stroke therapy; thrombectomy; thrombolysis; stroke in young adults; biomarkers in stroke; health-related quality of life after stroke

Special Issue Information

Dear Colleagues,

This Special Issue of Cells, titled "Molecular and Cellular Mechanisms of Ischemic Stroke", aims to provide a comprehensive overview of the complex pathophysiological processes underlying ischemic stroke at the molecular and cellular levels. Ischemic stroke remains a leading cause of death and long-term disability worldwide, yet effective therapeutic options are limited. Understanding the intricate interplay between neurons, glial cells, the neurovascular unit, immune responses, and systemic factors is essential for developing novel diagnostic markers and targeted therapies.

We welcome all original research articles, reviews, and communications focusing on this topic. Both in vitro and in vivo models, translational and human studies, as well as studies on rare causes of stroke are within the scope of this Special Issue. Contributions that highlight molecular pathways with clinical relevance are particularly welcome. 

Dr. Milani Deb-Chatterji
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 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-anonymized 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

  • ischemic stroke
  • neuroinflammation
  • blood–brain barrier
  • neurovascular unit
  • molecular targets for stroke therapy

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Published Papers (2 papers)

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Research

18 pages, 4527 KB  
Article
Reduced Cerebral Infarct Volume in Young UCP2−/− Mice and Preserved Synaptic Transmission by Genipin
by Gesine Reichart, Henrieke Koch, Tina Sellmann, Anne Einsle, Johannes Mayer, Robert Jaster, Timo Kirschstein, Falko Lange and Rüdiger Köhling
Cells 2026, 15(14), 1299; https://doi.org/10.3390/cells15141299 - 21 Jul 2026
Abstract
Cerebral ischemia–reperfusion injury is a key determinant of a poor outcome after stroke. The mitochondrial uncoupling protein 2 (UCP2) has been implicated in cerebral ischemia-reperfusion injury and in the outcome of ischemic stroke, although its role remains controversial. In C57BL/6J and B6.129S4-Ucp2 [...] Read more.
Cerebral ischemia–reperfusion injury is a key determinant of a poor outcome after stroke. The mitochondrial uncoupling protein 2 (UCP2) has been implicated in cerebral ischemia-reperfusion injury and in the outcome of ischemic stroke, although its role remains controversial. In C57BL/6J and B6.129S4-Ucp2tm1Lowl/J (UCP2−/−) mice, we analyzed cognitive function and lifespan. In an MCAO model induced for one hour, infarct volumes, neurological deficits, and gene expression patterns were determined after 24 h. The UCP2 inhibitor genipin was used in an oxygen-glucose deprivation (OGD) model to investigate synaptic transmission in the hippocampus. Compared to controls, UCP2−/− mice exhibited a reduced lifespan and displayed impaired cognition. However, in 6-month-old UCP2−/− mice, the infarct volume was reduced, primarily due to a smaller core size, but not in 18-month-old animals. In both strains, ischemia induced upregulation of antioxidant defense genes, including catalase and SOD1. In the ex vivo ODG model, synaptic transmission was depressed, but pretreatment with genipin prevented the tissue from this impairment. Our findings indicate an infarct-reducing effect of UCP2 deficiency, especially in young-adult mice, and, mechanistically, a neuroprotective effect by genipin in hippocampal slices. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Ischemic Stroke)
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18 pages, 5350 KB  
Article
FABP3 Aggravates Cerebral Ischemia–Reperfusion Injury by Promoting Mitochondrial Lipid Accumulation and Enhancing BAX-Dependent Apoptosis
by Yunsi Zheng, Anqi Luo, Kohji Fukunaga, Qibing Liu and Qingyun Guo
Cells 2026, 15(11), 1003; https://doi.org/10.3390/cells15111003 - 29 May 2026
Viewed by 540
Abstract
We previously demonstrated that fatty acid-binding protein 3 (FABP3) is significantly upregulated in ischemic neurons, and its inhibition mitigates ischemic brain injury in mice and attenuates mitochondrial damage under rotenone-induced oxidative stress. These findings suggest a potential role for FABP3 in mitochondrial dysfunction [...] Read more.
We previously demonstrated that fatty acid-binding protein 3 (FABP3) is significantly upregulated in ischemic neurons, and its inhibition mitigates ischemic brain injury in mice and attenuates mitochondrial damage under rotenone-induced oxidative stress. These findings suggest a potential role for FABP3 in mitochondrial dysfunction in ischemic neurons, although the underlying mechanism remains unclear. In this study, we further investigated the role of FABP3 in mitochondrial injury and apoptosis in ischemic neurons. Our findings indicated that FABP3 deficiency significantly decreased infarct volume following middle cerebral artery occlusion/reperfusion (MCAO/R) in mice, improved cognitive and spontaneous activity deficits, and suppressed BAX activation and mitochondrial translocation, caspase-3 activation, and cytochrome c release. In HT22 cells subjected to oxygen-glucose deprivation/reoxygenation (OGD/R), FABP3 deficiency increased cell viability, reduced apoptosis, and alleviated the loss of mitochondrial membrane potential. Conversely, FABP3 overexpression further exacerbated mitochondrial dysfunction and apoptosis, effects that were partially reversed by the BAX inhibitor BAI1. Furthermore, FABP3 overexpression promoted abnormal mitochondrial lipid accumulation and increased lipid peroxidation. Both the mitochondria-targeted antioxidant MitoQ and the ferroptosis inhibitor Ferrostatin-1 alleviated FABP3 overexpression-induced mitochondrial damage and apoptotic signaling. Collectively, our findings suggest that FABP3 is an important promoter of cerebral ischemia–reperfusion injury. FABP3 may aggravate ischemic neuronal injury by promoting abnormal mitochondrial lipid accumulation and lipid peroxidation, thereby enhancing BAX-dependent mitochondrial apoptotic signaling. Targeting FABP3 may provide a potential therapeutic strategy for neuroprotection in ischemic stroke. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Ischemic Stroke)
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