Nervous System Injury and Repair: From Molecular Mechanism to Therapeutic Perspectives

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: 28 February 2026 | Viewed by 409

Special Issue Editor


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Guest Editor
Center for Medical Research, The Second Xiangya Hospital of Central South University, Changsha 410011, China
Interests: nervous system injury; neuronal death; axon injury; oxidative stress; excitotoxicity; neuroinflammation; stroke; trauma

Special Issue Information

Dear Colleagues,

Nervous system injury is a leading risk factor for disability and death in the absence of effective treatment. The pathogeneses of neural damage are highly complex and involve factors such as energy deficiency, ion imbalance, and metabolic disorders. Following neural injury, a cascade of events including excitotoxicity, inflammation, and oxidative stress contributes to the death of neurons and non-neuronal cells (such as astrocytes and microglial cells) in the brain, ultimately resulting in outcomes like motor dysfunction, cognitive impairment, and other neurological deficits.

Using various of neural injury models helps investigate the cellular and molecular regulatory mechanisms underlying neural damage and provide neuroprotection strategies. However research progress and treatment efficacy remain limited for subsets of nervous system injuries. Therefore, further investigation into molecular targets and pharmacological neuroprotection is urgently needed.

Dr. Shuchao Wang
Guest Editor

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Keywords

  • nervous system injury
  • neuron
  • astrocytes
  • microglial cells
  • excitotoxicity
  • inflammation
  • oxidative stress
  • neuroprotection

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Published Papers (1 paper)

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Research

22 pages, 5859 KB  
Article
miR-21-5p Alleviates Retinal Ischemia–Reperfusion Injury by Inhibiting M1 Polarization of Microglia via Suppression of STAT3 Signaling
by Liangshi Qin, Junle Liao, Cheng Tan, Can Liu, Wenjia Shi and Dan Chen
Biomedicines 2025, 13(10), 2456; https://doi.org/10.3390/biomedicines13102456 - 9 Oct 2025
Viewed by 251
Abstract
Background/Objectives: Retinal ischemia–reperfusion (I/R) injury is a common mechanism in glaucoma, diabetic retinopathy, and retinal vein occlusion, leading to progressive loss of retinal ganglion cells (RGCs). This study investigates the regulatory role of miR-21-5p and its interaction with Signal Transducer and Activator [...] Read more.
Background/Objectives: Retinal ischemia–reperfusion (I/R) injury is a common mechanism in glaucoma, diabetic retinopathy, and retinal vein occlusion, leading to progressive loss of retinal ganglion cells (RGCs). This study investigates the regulatory role of miR-21-5p and its interaction with Signal Transducer and Activator of Transcription 3 (STAT3) in retinal I/R injury. Methods: An acute intraocular hypertension (AIH) rat model was used to induce retinal I/R. The interaction between miR-21-5p and STAT3 was examined by dual-luciferase reporter assays. miR-21-5p and STAT3 expression were quantified by qRT-PCR and Western blotting. Retinal morphology, microglial polarization, and RGC survival were assessed by H&E staining and immunofluorescence. In vitro, microglia and RGCs were subjected to oxygen–glucose deprivation/reperfusion (OGD/R), and microglial-conditioned media (MCM) were applied to RGCs. Results: (1) miR-21-5p ameliorated AIH-induced retinal damage in vivo. (2) Overexpression of miR-21-5p inhibits M1 polarization of RM cultured in vitro. (3) MCM from miR-21-5p-overexpressing microglia attenuated OGD/R-induced RGC death. (4) miR-21-5p downregulates STAT3 expression to inhibit RM M1 polarization. (5) miR-21-5p down-regulation of STAT3 levels inhibits M1 polarization and reduces apoptosis of RGCs in retinal microglia of AIH rats. Conclusions: miR-21-5p alleviates retinal I/R injury by restraining microglial M1 polarization through direct repression of STAT3, thereby promoting RGC survival. These findings identify the miR-21-5p/STAT3 axis as a potential therapeutic target for ischemic retinal diseases. Full article
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