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

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Cellular Biochemistry".

Deadline for manuscript submissions: 31 December 2024 | Viewed by 5078

Special Issue Editor

Dr. Yuchuan Ding

E-Mail Website
Guest Editor
Department of Neurosurgery, Wayne State University School of Medicine, Detroit, MI 48201, USA
Interests: stroke; neuroprotection; brain circulation; conditioning medicine; exercise; ischemia and reperfusion injury; stress; vascular diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are very happy to invite submissions to the esteemed journal Biomolecules for a Special Issue entitled "Molecular and Cellular Mechanisms of Ischemic Stroke." This Special Issue seeks to highlight cutting-edge research, reviews, perspectives, and experimental methodologies that illuminate the complex nature of neurocognitive disorders, particularly focusing on the etiology of stroke and the innovations in recovery and rehabilitation processes.

The goal of this Special Issue is to promote a rich, interdisciplinary forum for sharing and discussing the latest discoveries and developments in the field of stroke research. We aim to explore the molecular and cellular foundations of ischemic stroke and to advance the development of emerging therapeutic interventions. Contributions may come from a diverse array of scientific areas, including neurobiology, neuroscience, clinical neurology, neurosurgery, rehabilitation medicine, molecular biology, and genetics.

We are looking forward to your insightful contributions to deepen our understanding and encourage innovation in the field of ischemic stroke research and therapy.

Dr. Yuchuan Ding
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. Biomolecules 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 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
  • neuroprotection
  • brain circulation
  • rehabilitation medicine

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Published Papers (5 papers)

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Research

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20 pages, 8616 KiB  
Article
Ischemic Postconditioning Regulates New Cell Death Mechanisms in Stroke: Disulfidptosis
by Shanpeng Liu, Qike Wu, Can Xu, Liping Wang, Jialing Wang, Cuiying Liu and Heng Zhao
Biomolecules 2024, 14(11), 1390; https://doi.org/10.3390/biom14111390 - 31 Oct 2024
Viewed by 617
Abstract
Background and Objective: Stroke poses a critical health issue without effective neuroprotection. We explore ischemic postconditioning’s (IPostC) potential to mitigate stroke-induced brain injury, focusing on its interaction with disulfidptosis, a novel cell death pathway marked by protein disulfide accumulation. We aim to clarify [...] Read more.
Background and Objective: Stroke poses a critical health issue without effective neuroprotection. We explore ischemic postconditioning’s (IPostC) potential to mitigate stroke-induced brain injury, focusing on its interaction with disulfidptosis, a novel cell death pathway marked by protein disulfide accumulation. We aim to clarify IPostC’s protective mechanisms against stroke through gene sequencing and experimental analysis in mice. Methods: Through our initial investigation, we identified 27 disulfidptosis-related genes (DRGs) and uncovered their interactions. Additionally, differential gene analysis revealed 11 potential candidate genes that are linked to disulfidptosis, stroke, and IPostC. Our comprehensive study employed various analytical approaches, including machine learning, functional enrichment analysis, immune analysis, drug sensitivity analysis, and qPCR experiments, to gain insights into the molecular mechanisms underlying these processes. Results: Our study identified and expanded the list of disulfidptosis-related genes (DRGs) critical to stroke, revealing key genes and their interactions. Through bioinformatics analyses, including PCA, UMAP, and differential gene expression, we were able to differentiate the effects of stroke from those of postconditioning, identifying Peroxiredoxin 1 (PRDX1) as a key gene of interest. GSEA highlighted PRDX1’s involvement in protective pathways against ischemic damage, while its correlations with various proteins suggest a broad impact on stroke pathology. Constructing a ceRNA network and analyzing drug sensitivities, we explored PRDX1’s regulatory mechanisms, proposing novel therapeutic avenues. Additionally, our immune infiltration analysis linked PRDX1 to key immune cells, underscoring its dual role in stroke progression and recovery. PRDX1 is identified as a key target in ischemic stroke based on colocalization analysis, which revealed that PRDX1 and ischemic stroke share the causal variant rs17522918. The causal relationship between PRDX1-related methylation sites (cg02631906 and cg08483560) and the risk of ischemic stroke further validates PRDX1 as a crucial target. Conclusions: These results suggest that the DRGs are interconnected with various cell death pathways and immune processes, potentially contributing to IPostC regulating cell death mechanisms in stroke. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Ischemic Stroke)
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Review

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26 pages, 2960 KiB  
Review
Exosomes in Central Nervous System Diseases: A Comprehensive Review of Emerging Research and Clinical Frontiers
by Jingrun Li, Jiahao Song, Lina Jia, Mengqi Wang, Xunming Ji, Ran Meng and Da Zhou
Biomolecules 2024, 14(12), 1519; https://doi.org/10.3390/biom14121519 (registering DOI) - 27 Nov 2024
Abstract
Exosomes, nano-sized lipid bilayer vesicles, have garnered significant attention as mediators of cell communication, particularly within the central nervous system (CNS). Their unique properties, including high stability, low immunogenicity, and the ability to traverse the blood-brain barrier (BBB), position them as promising tools [...] Read more.
Exosomes, nano-sized lipid bilayer vesicles, have garnered significant attention as mediators of cell communication, particularly within the central nervous system (CNS). Their unique properties, including high stability, low immunogenicity, and the ability to traverse the blood-brain barrier (BBB), position them as promising tools for understanding and addressing CNS diseases. This comprehensive review delves into the biogenesis, properties, composition, functions, and isolation of exosomes, with a particular focus on their roles in cerebrovascular diseases, neurodegenerative disorders, and CNS tumors. Exosomes are involved in key pathophysiological processes in the CNS, including angiogenesis, inflammation, apoptosis, and cellular microenvironment modification. They demonstrate promise in mitigating ischemic injury, regulating inflammatory responses, and providing neuroprotection across various CNS conditions. Furthermore, exosomes carry distinct biomolecules, offering a novel method for the early diagnosis and monitoring of CNS diseases. Despite their potential, challenges such as complex extraction processes, the heterogeneity of exosomal contents, and targeted delivery limitations hinder their clinical application. Nevertheless, exosomes hold significant promise for advancing our understanding of CNS diseases and developing novel therapeutic strategies. This manuscript significantly contributes to the field by highlighting exosomes’ potential in advancing our understanding of CNS diseases, underscoring their unique value in developing novel therapeutic strategies and mediating cellular communication. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Ischemic Stroke)
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15 pages, 733 KiB  
Review
Beyond Pharmacology: The Biological Mechanisms of Remote Ischemic Conditioning in Cerebrovascular Disease
by Linhui Qin, Fang Tong, Sijie Li and Changhong Ren
Biomolecules 2024, 14(11), 1408; https://doi.org/10.3390/biom14111408 - 5 Nov 2024
Viewed by 613
Abstract
Cerebrovascular diseases (CVDs), comprising predominantly ischemic stroke and chronic cerebral hypoperfusion (CCH), are a significant threat to global health, often leading to disability and mortality. Remote ischemic conditioning (RIC) has emerged as a promising, non-pharmacological strategy to combat CVDs by leveraging the body’s [...] Read more.
Cerebrovascular diseases (CVDs), comprising predominantly ischemic stroke and chronic cerebral hypoperfusion (CCH), are a significant threat to global health, often leading to disability and mortality. Remote ischemic conditioning (RIC) has emerged as a promising, non-pharmacological strategy to combat CVDs by leveraging the body’s innate defense mechanisms. This review delves into the neuroprotective mechanisms of RIC, categorizing its effects during the acute and chronic phases of stroke recovery. It also explores the synergistic potential of RIC when combined with other therapeutic strategies, such as pharmacological treatments and physical exercise. Additionally, this review discusses the pathways through which peripheral transmission can confer central neuroprotection. This review concludes by addressing the challenges regarding and future directions for RIC, emphasizing the need for standardized protocols, biomarker identification, and expanded clinical trials to fully realize its therapeutic potential. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Ischemic Stroke)
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14 pages, 4553 KiB  
Review
Phosphatidylserine: A Novel Target for Ischemic Stroke Treatment
by Jiaqi Guo, Jiachen He, Shuaili Xu, Xi Chen, Zhanwei Zhu, Xunming Ji and Di Wu
Biomolecules 2024, 14(10), 1293; https://doi.org/10.3390/biom14101293 - 12 Oct 2024
Viewed by 1297
Abstract
Over the past 40 years, research has heavily emphasized stroke treatments that directly target ischemic cascades after stroke onset. Much attention has focused on studying neuroprotective drugs targeting one aspect of the ischemic cascade. However, the single-target therapeutic approach resulted in minimal clinical [...] Read more.
Over the past 40 years, research has heavily emphasized stroke treatments that directly target ischemic cascades after stroke onset. Much attention has focused on studying neuroprotective drugs targeting one aspect of the ischemic cascade. However, the single-target therapeutic approach resulted in minimal clinical benefit and poor outcomes in patients. Considering the ischemic cascade is a multifaceted and complex pathophysiological process with many interrelated pathways, the spotlight is now shifting towards the development of neuroprotective drugs that affect multiple aspects of the ischemic cascade. Phosphatidylserine (PS), known as the “eat-me” signal, is a promising candidate. PS is involved in many pathophysiological changes in the central nervous system after stroke onset, including apoptosis, inflammation, coagulation, and neuronal regeneration. Moreover, PS might also exert various roles in different phases after stroke onset. In this review, we describe the synthesis, regulation, and function of PS under physiological conditions. Furthermore, we also summarize the different roles of PS after stroke onset. More importantly, we also discuss several treatment strategies that target PS. We aim to advocate a novel stroke care strategy by targeting PS through a translational perspective. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Ischemic Stroke)
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14 pages, 1007 KiB  
Review
Role of Specificity Protein 1 (SP1) in Cardiovascular Diseases: Pathological Mechanisms and Therapeutic Potentials
by Jie Ding, Aminah I. Fayyaz, Yuchuan Ding, Dandan Liang and Ming Luo
Biomolecules 2024, 14(7), 807; https://doi.org/10.3390/biom14070807 - 7 Jul 2024
Viewed by 1665
Abstract
In mammals, specificity protein 1 (SP1) was the first Cys2-His2 zinc finger transcription factor to be isolated within the specificity protein and Krüppel-like factor (Sp/KLF) gene family. SP1 regulates gene expression by binding to Guanine–Cytosine (GC)-rich sequences on promoter regions of target genes, [...] Read more.
In mammals, specificity protein 1 (SP1) was the first Cys2-His2 zinc finger transcription factor to be isolated within the specificity protein and Krüppel-like factor (Sp/KLF) gene family. SP1 regulates gene expression by binding to Guanine–Cytosine (GC)-rich sequences on promoter regions of target genes, affecting various cellular processes. Additionally, the activity of SP1 is markedly influenced by posttranslational modifications, such as phosphorylation, acetylation, glycosylation, and proteolysis. SP1 is implicated in the regulation of apoptosis, cell hypertrophy, inflammation, oxidative stress, lipid metabolism, plaque stabilization, endothelial dysfunction, fibrosis, calcification, and other pathological processes. These processes impact the onset and progression of numerous cardiovascular disorders, including coronary heart disease, ischemia-reperfusion injury, cardiomyopathy, arrhythmia, and vascular disease. SP1 emerges as a potential target for the prevention and therapeutic intervention of cardiac ailments. In this review, we delve into the biological functions, pathophysiological mechanisms, and potential clinical implications of SP1 in cardiac pathology to offer valuable insights into the regulatory functions of SP1 in heart diseases and unveil novel avenues for the prevention and treatment of cardiovascular conditions. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Ischemic Stroke)
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