医学最新文献

{"title":"Enhancing neural stem cell integration in the injured spinal cord through targeted PTEN modulation.","authors":"Simay Genişcan, Hee Hwan Park, Hyung Soon Kim, Seokjin Yoo, Hyunmi Kim, Byeong Seong Jang, Dong Hoon Hwang, Kevin K Park, Byung Gon Kim","doi":"10.4103/NRR.NRR-D-24-00455","DOIUrl":"10.4103/NRR.NRR-D-24-00455","url":null,"abstract":"<p><p>JOURNAL/nrgr/04.03/01300535-202604000-00039/figure1/v/2025-06-30T060627Z/r/image-tiff Spinal cord injury results in permanent loss of neurological functions due to severance of neural networks. Transplantation of neural stem cells holds promise to repair disrupted connections. Yet, ensuring the survival and integration of neural stem cells into the host neural circuit remains a formidable challenge. Here, we investigated whether modifying the intrinsic properties of neural stem cells could enhance their integration post-transplantation. We focused on phosphatase and tensin homolog (PTEN), a well-characterized tumor suppressor known to critically regulate neuronal survival and axonal regeneration. By deleting Pten in mouse neural stem cells, we observed increased neurite outgrowth and enhanced resistance to neurotoxic environments in culture. Upon transplantation into injured spinal cords, Pten-deficient neural stem cells exhibited higher survival and more extensive rostrocaudal distribution. To examine the potential influence of partial PTEN suppression, rat neural stem cells were treated with short hairpin RNA targeting PTEN, and the PTEN knockdown resulted in significant improvements in neurite growth, survival, and neurosphere motility in vitro . Transplantation of shPTEN-treated neural stem cells into the injured spinal cord also led to an increase in graft survival and migration to an extent similar to that of complete deletion. Moreover, PTEN suppression facilitated neurite elongation from NSC-derived neurons migrating from the lesion epicenter. These findings suggest that modifying intrinsic signaling pathways, such as PTEN, within neural stem cells could bolster their therapeutic efficacy, offering potential avenues for future regenerative strategies for spinal cord injury.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1586-1594"},"PeriodicalIF":5.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuropsychiatric symptoms and apolipoprotein E genotypes in neurocognitive disorders.","authors":"Madia Lozupone, Ivana Leccisotti, Anita Mollica, Giuseppe Berardino, Maria Claudia Moretti, Mario Altamura, Antonello Bellomo, Antonio Daniele, Vittorio Dibello, Vincenzo Solfrizzi, Emanuela Resta, Francesco Panza","doi":"10.4103/NRR.NRR-D-24-01274","DOIUrl":"10.4103/NRR.NRR-D-24-01274","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Complex genetic relationships between neurodegenerative disorders and neuropsychiatric symptoms have been shown, suggesting shared pathogenic mechanisms and emphasizing the potential for developing common therapeutic targets. Apolipoprotein E ( APOE ) genotypes and their corresponding protein (ApoE) isoforms may influence the biophysical properties of the cell membrane lipid bilayer. However, the role of APOE in central nervous system pathophysiology extended beyond its lipid transport function. In the present review article, we analyzed the links existing between APOE genotypes and the neurobiology of neuropsychiatric symptoms in neurodegenerative and vascular diseases. APOE genotypes ( APOE ε2, APOE ε3, and APOE ε4) were implicated in common mechanisms underlying a wide spectrum of neurodegenerative diseases, including sporadic Alzheimer's disease, synucleinopathies such as Parkinson's disease and Lewy body disease, stroke, and traumatic brain injury. These shared pathways often involved neuroinflammation, abnormal protein accumulation, or responses to acute detrimental events. Across these conditions, APOE variants are believed to contribute to the modulation of inflammatory responses, the regulation of amyloid and tau pathology, as well as the clearance of proteins such as α-synuclein. The bidirectional interactions among ApoE, amyloid and mitochondrial metabolism, immunomodulatory effects, neuronal repair, and remodeling underscored the complexity of ApoE's role in neuropsychiatric symptoms associated with these conditions since from early phases of cognitive impairment such as mild cognitive impairment and mild behavioral impairment. Besides ApoE-specific isoforms' link to increased neuropsychiatric symptoms in Alzheimer's disease (depression, psychosis, aberrant motor behaviors, and anxiety, not apathy), the APOE ε4 genotype was also considered a significant genetic risk factor for Lewy body disease and its worse cognitive outcomes. Conversely, the APOE ε2 variant has been observed not to exert a protective effect equally in all neurodegenerative diseases. Specifically, in Lewy body disease, this variant may delay disease onset, paralleling its protective role in Alzheimer's disease, although its role in frontotemporal dementia is uncertain. The APOE ε4 genotype has been associated with adverse cognitive outcomes across other various neurodegenerative conditions. In Parkinson's disease, the APOE ε4 allele significantly impacted cognitive performance, increasing the risk of developing dementia, even in cases of pure synucleinopathies with minimal co-pathology from Alzheimer's disease. Similarly, in traumatic brain injury, recovery rates varied, with APOE ε4 carriers demonstrating a greater risk of poor long-term cognitive outcomes and elevated levels of neuropsychiatric symptoms. Furthermore, APOE ε4 influenced the age of onset and severity of stroke, as well as the likelihood of developing stroke-associated dementia, potentially due ","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1528-1541"},"PeriodicalIF":5.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143720921","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Brain-derived extracellular vesicles: A promising avenue for Parkinson's disease pathogenesis, diagnosis, and treatment.","authors":"Shurui Zhang, Jingwen Li, Xinyu Hu, Hanshu Liu, Qinwei Yu, Guiying Kuang, Long Liu, Danfang Yu, Zhicheng Lin, Nian Xiong","doi":"10.4103/NRR.NRR-D-24-01262","DOIUrl":"10.4103/NRR.NRR-D-24-01262","url":null,"abstract":"&lt;p&gt;&lt;p&gt;The misfolding, aggregation, and deposition of alpha-synuclein into Lewy bodies are pivotal events that trigger pathological changes in Parkinson's disease. Extracellular vesicles are nanosized lipid-bilayer vesicles secreted by cells that play a crucial role in intercellular communication due to their diverse cargo. Among these, brain-derived extracellular vesicles, which are secreted by various brain cells such as neurons, glial cells, and Schwann cells, have garnered increasing attention. They serve as a promising tool for elucidating Parkinson's disease pathogenesis and for advancing diagnostic and therapeutic strategies. This review highlights the recent advancements in our understanding of brain-derived extracellular vesicles released into the blood and their role in the pathogenesis of Parkinson's disease, with specific emphasis on their involvement in the aggregation and spread of alpha-synuclein. Brain-derived extracellular vesicles contribute to disease progression through multiple mechanisms, including autophagy-lysosome dysfunction, neuroinflammation, and oxidative stress, collectively driving neurodegeneration in Parkinson's disease. Their application in Parkinson's disease diagnosis is a primary focus of this review. Recent studies have demonstrated that brain-derived extracellular vesicles can be isolated from peripheral blood samples, as they carry α-synuclein and other key biomarkers such as DJ-1 and various microRNAs. These findings highlight the potential of brain-derived extracellular vesicles, not only for the early diagnosis of Parkinson's disease but also for disease progression monitoring and differential diagnosis. Additionally, an overview of explorations into the potential therapeutic applications of brain-derived extracellular vesicles for Parkinson's disease is provided. Therapeutic strategies targeting brain-derived extracellular vesicles involve modulating the release and uptake of pathological alpha-synuclein -containing brain-derived extracellular vesicles to inhibit the spread of the protein. Moreover, brain-derived extracellular vesicles show immense promise as therapeutic delivery vehicles capable of transporting drugs into the central nervous system. Importantly, brain-derived extracellular vesicles also play a crucial role in neural regeneration by promoting neuronal protection, supporting axonal regeneration, and facilitating myelin repair, further enhancing their therapeutic potential in Parkinson's disease and other neurological disorders. Further clarification is needed of the methods for identifying and extracting brain-derived extracellular vesicles, and large-scale cohort studies are necessary to validate the accuracy and specificity of these biomarkers. Future research should focus on systematically elucidating the unique mechanistic roles of brain-derived extracellular vesicles, as well as their distinct advantages in the clinical translation of methods for early detection and therapeutic devel","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1447-1467"},"PeriodicalIF":5.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144028795","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unfolded protein response in endoplasmic reticulum stress associated with retinal degenerative diseases: A promising therapeutic target.","authors":"Hongbing Zhang, Yalin Mu, Hongsong Li, Xiaogang Li","doi":"10.4103/NRR.NRR-D-24-01124","DOIUrl":"10.4103/NRR.NRR-D-24-01124","url":null,"abstract":"<p><p>The unfolded protein response is a cellular pathway activated to maintain proteostasis and prevent cell death when the endoplasmic reticulum is overwhelmed by unfolded proteins. However, if the unfolded protein response fails to restore endoplasmic reticulum homeostasis, it can trigger pro-inflammatory and pro-death signals, which are implicated in various malignancies and are currently being investigated for their role in retinal degenerative diseases. This paper reviews the role of the unfolded protein responsein addressing endoplasmic reticulumstress in retinal degenerative diseases. The accumulation of ubiquitylated misfolded proteins can lead to rapid destabilization of the proteome and cellular demise. Targeting endoplasmic reticulum stress to alleviate retinal pathologies involves multiple strategies, including the use of chemical chaperones such as 4-phenylbutyric acid and tauroursodeoxycholic acid, which enhance protein folding and reduce endoplasmic reticulum stress. Small molecule modulators that influence endoplasmic reticulum stress sensors, including those that increase the expression of the endoplasmic reticulum stress regulator X-box binding protein 1, are also potential therapeutic agents. Additionally, inhibitors of the RNAse activity of inositol-requiring transmembrane kinase/endoribonuclease 1, a key endoplasmic reticulum stress sensor, represent another class of drugs that could prevent the formation of toxic aggregates. The activation of nuclear receptors, such as PPAR and FXR, may also help mitigate ER stress. Furthermore, enhancing proteolysis through the induction of autophagy or the inhibition of deubiquitinating enzymes can assist in clearing misfolded proteins. Combination treatments that involve endoplasmic-reticulum-stress-targeting drugs and gene therapies are also being explored. Despite these potential therapeutic strategies, significant challenges remain in targeting endoplasmic reticulum stress for the treatment of retinal degeneration, and further research is essential to elucidate the mechanisms underlying human retinal diseases and to develop effective, well-tolerated drugs. The use of existing drugs that target inositol-requiring transmembrane kinase/endoribonuclease 1 and X-box binding protein 1 has been associated with adverse side effects, which have hindered their clinical translation. Moreover, signaling pathways downstream of endoplasmic reticulum stress sensors can contribute to therapy resistance. Addressing these limitations is crucial for developing drugs that can be effectively used in treating retinal dystrophies. In conclusion, while the unfolded protein response is a promising therapeutic target in retinal degenerative diseases, additional research and development efforts are imperative to overcome the current limitations and improve patient outcomes.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1339-1352"},"PeriodicalIF":5.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144333608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Noradrenergic excitation of astrocytes supports cognitive reserve.","authors":"Robert Zorec, Alexei Verkhratsky","doi":"10.4103/NRR.NRR-D-24-01395","DOIUrl":"https://doi.org/10.4103/NRR.NRR-D-24-01395","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":"21 4","pages":"1546-1547"},"PeriodicalIF":5.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144528965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Determinants of alpha-synuclein pathogenesis in Parkinson's disease.","authors":"Oriol Bárcenas, Marc Estivill-Alonso, Salvador Ventura","doi":"10.4103/NRR.NRR-D-24-01357","DOIUrl":"10.4103/NRR.NRR-D-24-01357","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1568-1569"},"PeriodicalIF":5.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143493001","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Different roles of astrocytes in the blood-brain barrier during the acute and recovery phases of stroke.","authors":"Jialin Cheng, Yuxiao Zheng, Fafeng Cheng, Chunyu Wang, Jinhua Han, Haojia Zhang, Xin Lan, Chuxin Zhang, Xueqian Wang, Qingguo Wang, Changxiang Li","doi":"10.4103/NRR.NRR-D-24-01417","DOIUrl":"10.4103/NRR.NRR-D-24-01417","url":null,"abstract":"<p><p>Ischemic stroke, a frequently occurring form of stroke, is caused by obstruction of cerebral blood flow, which leads to ischemia, hypoxia, and necrosis of local brain tissue. After ischemic stroke, both astrocytes and the blood-brain barrier undergo morphological and functional transformations. However, the interplay between astrocytes and the blood-brain barrier has received less attention. This comprehensive review explores the physiological and pathological morphological and functional changes in astrocytes and the blood-brain barrier in ischemic stroke. Post-stroke, the structure of endothelial cells and peripheral cells undergoes alterations, causing disruption of the blood-brain barrier. This disruption allows various pro-inflammatory factors and chemokines to cross the blood-brain barrier. Simultaneously, astrocytes swell and primarily adopt two phenotypic states: A1 and A2, which exhibit different roles at different stages of ischemic stroke. During the acute phase, A1 reactive astrocytes secrete vascular endothelial growth factor, matrix metalloproteinases, lipid carrier protein-2, and other cytokines, exacerbating damage to endothelial cells and tight junctions. Conversely, A2 reactive astrocytes produce pentraxin 3, Sonic hedgehog, angiopoietin-1, and other protective factors for endothelial cells. Furthermore, astrocytes indirectly influence blood-brain barrier permeability through ferroptosis and exosomes. In the middle and late (recovery) stages of ischemic stroke, A1 and A2 astrocytes show different effects on glial scar formation. A1 astrocytes promote glial scar formation and inhibit axon growth via glial fibrillary acidic protein, chondroitin sulfate proteoglycans, and transforming growth factor-β. In contrast, A2 astrocytes facilitate axon growth through platelet-derived growth factor, playing a crucial role in vascular remodeling. Therefore, enhancing our understanding of the pathological changes and interactions between astrocytes and the blood-brain barrier is a vital therapeutic target for preventing further brain damage in acute stroke. These insights may pave the way for innovative therapeutic strategies for ischemic stroke.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1359-1372"},"PeriodicalIF":5.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144333554","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroglobin: A promising candidate to treat neurological diseases.","authors":"Ivan Millan Yañez, Isabel Torres-Cuevas, Marisol Corral-Debrinski","doi":"10.4103/NRR.NRR-D-24-01503","DOIUrl":"10.4103/NRR.NRR-D-24-01503","url":null,"abstract":"<p><p>Neurodevelopmental and neurodegenerative illnesses constitute a global health issue and a foremost economic burden since they are a large cause of incapacity and death worldwide. Altogether, the burden of neurological disorders has increased considerably over the past 30 years because of population aging. Overall, neurological diseases significantly impair cognitive and motor functions and their incidence will increase as societies age and the world's population continues to grow. Autism spectrum disorder, motor neuron disease, encephalopathy, epilepsy, stroke, ataxia, Alzheimer's disease, amyotrophic lateral sclerosis, Huntington's disease, and Parkinson's disease represent a non-exhaustive list of neurological illnesses. These affections are due to perturbations in cellular homeostasis leading to the progressive injury and death of neurons in the nervous system. Among the common features of neurological handicaps, we find protein aggregation, oxidative stress, neuroinflammation, and mitochondrial impairment in the target tissues, e.g., the brain, cerebellum, and spinal cord. The high energy requirements of neurons and their inability to produce sufficient adenosine triphosphate by glycolysis, are responsible for their dependence on functional mitochondria for their integrity. Reactive oxygen species, produced along with the respiration process within mitochondria, can lead to oxidative stress, which compromises neuronal survival. Besides having an essential role in energy production and oxidative stress, mitochondria are indispensable for an array of cellular processes, such as amino acid metabolism, iron-sulfur cluster biosynthesis, calcium homeostasis, intrinsic programmed cell death (apoptosis), and intraorganellar signaling. Despite the progress made in the last decades in the understanding of a growing number of genetic and molecular causes of central nervous diseases, therapies that are effective to diminish or halt neuronal dysfunction/death are rare. Given the genetic complexity responsible for neurological disorders, the development of neuroprotective strategies seeking to preserve mitochondrial homeostasis is a realistic challenge to lastingly diminish the harmful evolution of these pathologies and so to recover quality of life. A promising candidate is the neuroglobin, a globin superfamily member of 151 amino acids, which is found at high levels in the brain, the eye, and the cerebellum. The protein, which localizes to mitochondria, is involved in electron transfer, oxygen storage and defence against oxidative stress; hence, possessing neuroprotective properties. This review surveys up-to-date knowledge and emphasizes on existing investigations regarding neuroglobin physiological functions, which remain since its discovery in 2000 under intense debate and the possibility of using neuroglobin either by gene therapy or its direct delivery into the brain to treat neurological disorders.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1292-1303"},"PeriodicalIF":5.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144333584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stem cell repair strategies for epilepsy.","authors":"Xiao Ma, Zitong Wang, Yinuo Niu, Jie Zhao, Xiaorui Wang, Xuan Wang, Fang Yang, Dong Wei, Zhongqing Sun, Wen Jiang","doi":"10.4103/NRR.NRR-D-24-01337","DOIUrl":"10.4103/NRR.NRR-D-24-01337","url":null,"abstract":"<p><p>Epilepsy is a serious neurological disorder; however, the effectiveness of current medications is often suboptimal. Recently, stem cell technology has demonstrated remarkable therapeutic potential in addressing various neurological diseases, igniting interest in its applicability for epilepsy treatment. This comprehensive review summarizes different therapeutic approaches utilizing various types of stem cells. Preclinical experiments have explored the use and potential therapeutic effects of mesenchymal stem cells, including genetically modified variants. Clinical trials involving patient-derived mesenchymal stem cells have shown promising results, with reductions in the frequency of epileptic seizures and improvements in neurological, cognitive, and motor functions reported. Another promising therapeutic strategy involves neural stem cells. These cells can be cultured outside the body and directed to differentiate into specific cell types. The transplant of neural stem cells has the potential to replace lost inhibitory interneurons, providing a novel treatment avenue for epilepsy. Embryonic stem cells are characterized by their significant capacity for self-renewal and their ability to differentiate into any type of somatic cell. In epilepsy treatment, embryonic stem cells can serve three primary functions: neuron regeneration, the maintenance of cellular homeostasis, and restorative activity. One notable strategy involves differentiating embryonic stem cells into γ-aminobutyric acidergic neurons for transplantation into lesion sites. This approach is currently undergoing clinical trials and could be a breakthrough in the treatment of refractory epilepsy. Induced pluripotent stem cells share the same genetic background as the donor, thereby reducing the risk of immune rejection and addressing ethical concerns. However, research on induced pluripotent stem cell therapy remains in the preclinical stage. Despite the promise of stem cell therapies for epilepsy, several limitations must be addressed. Safety concerns persist, including issues such as tumor formation, and the low survival rate of transplanted cells remains a significant challenge. Additionally, the high cost of these treatments may be prohibitive for some patients. In summary, stem cell therapy shows considerable promise in managing epilepsy, but further research is needed to overcome its existing limitations and enhance its clinical applicability.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1428-1446"},"PeriodicalIF":5.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144333603","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitophagy: A key regulator in the pathophysiology and treatment of spinal cord injury.","authors":"Qiuyang Gu, Shengye Yuan, Yumei An, Wenyue Sun, Mingyuan Xu, Mengchun Xue, Xianzhe Li, Chao Liu, Haiyan Shan, Mingyang Zhang","doi":"10.4103/NRR.NRR-D-24-01029","DOIUrl":"https://doi.org/10.4103/NRR.NRR-D-24-01029","url":null,"abstract":"<p><p>Mitophagy is closely associated with the pathogenesis of secondary spinal cord injury. Abnormal mitophagy may contribute significantly to secondary spinal cord injury, leading to the impaired production of adenosine triphosphate, ion imbalance, the excessive production of reactive oxygen species, neuroinflammation, and neuronal cell death. Therefore, maintaining an appropriate balance of mitophagy is crucial when treating spinal cord injury, as both excessive and insufficient mitophagy can impede recovery. In this review, we summarize the pathological changes associated with spinal cord injury, the mechanisms of mitophagy, and the direct and indirect relationships between mitophagy and spinal cord injury. We also consider therapeutic approaches that target mitophagy for the treatment of spinal cord injury, including ongoing clinical trials and other innovative therapies, such as use of stem cells, nanomaterials, and small molecule polymers. Finally, we highlight the current challenges facing this field and suggest potential directions for future research. The aim of our review is to provide a theoretical reference for future studies targeting mitophagy in the treatment of spinal cord injury.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":"21 4","pages":"1396-1408"},"PeriodicalIF":5.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144528962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}