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1.
J Pain Res ; 17: 2165-2190, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38910593

RESUMO

Background: The increasing utilization of endoscopic lumbar discectomy (ELD) in spinal surgery has sparked widespread interest and research. This study utilizes bibliometric analysis to identify current research trends and advancements in this innovative surgical technique, with the goal of informing and improving surgical practices. Methods: We retrieved relevant literature on ELD from the Science Citation Index Expanded (SCI-Expanded) within the Web of Science Core Collection (WoSCC) database as research samples. Various visualization tools, such as VOSviewer, CiteSpace, Scimago Graphica, Pajek, and online bibliometric platform, were employed to generate scientific knowledge maps for the purpose of visual presentation and data analysis. Results: Over the past two decades, there has been significant progress in the research related to ELD, particularly since 2016. China has emerged as the most productive country, while South Korea and the United States have exerted greater academic influence. Tongji University has contributed the highest number of research output, while academic achievements published by Wooridul Spine Hospital are highly esteemed by scholars. Lee SH and Ruetten S are the most prolific author and the most highly cited author, respectively. World Neurosurg has published the highest number of publications, while Spine has become the most influential journal. Clinical Neurology and Surgery are the primary subject categories. Research in this field primarily revolves around improving ELD techniques, evaluating postoperative efficacy and prognosis prediction, studying complications and risk factors, as well as comparative research with other surgical techniques. Keywords such as risk factors, LDH, PETD, lumbar spinal stenosis, degeneration, recurrent herniation, laminectomy, local anesthesia, and foraminoplasty highlight the current research hotspots and future cutting-edge trends. Conclusion: This study employed bibliometric analysis to elucidate the research hotspots and frontiers in ELD. The findings have significant implications for advancing research and development in this field.

2.
Cell Death Differ ; 25(8): 1503-1516, 2018 08.
Artigo em Inglês | MEDLINE | ID: mdl-29396549

RESUMO

In response to stroke, astrocytes become reactive astrogliosis and are a major component of a glial scar. This results in the formation of both a physical and chemical (production of chondroitin sulfate proteoglycans) barrier, which prevent neurite regeneration that, in turn, interferes with functional recovery. However, the mechanisms of reactive astrogliosis and glial scar formation are poorly understood. In this work, we hypothesized that repulsive guidance molecule a (RGMa) regulate reactive astrogliosis and glial scar formation. We first found that RGMa was strongly expressed by reactive astrocytes in the glial scar in a rat model of middle cerebral artery occlusion/reperfusion. Genetic or pharmacologic inhibition of RGMa in vivo resulted in a strong reduction of reactive astrogliosis and glial scarring as well as in a pronounced improvement in functional recovery. Furthermore, we showed that transforming growth factor ß1 (TGFß1) stimulated RGMa expression through TGFß1 receptor activin-like kinase 5 (ALK5) in primary cultured astrocytes. Knockdown of RGMa abrogated key steps of reactive astrogliosis and glial scar formation induced by TGFß1, including cellular hypertrophy, glial fibrillary acidic protein upregulation, cell migration, and CSPGs secretion. Finally, we demonstrated that RGMa co-immunoprecipitated with ALK5 and Smad2/3. TGFß1-induced ALK5-Smad2/3 interaction and subsequent phosphorylation of Smad2/3 were impaired by RGMa knockdown. Taken together, we identified that after stroke, RGMa promotes reactive astrogliosis and glial scar formation by forming a complex with ALK5 and Smad2/3 to promote ALK5-Smad2/3 interaction to facilitate TGFß1/Smad2/3 signaling, thereby inhibiting neurological functional recovery. RGMa may be a new therapeutic target for stroke.


Assuntos
Proteínas de Membrana/metabolismo , Proteínas do Tecido Nervoso/metabolismo , Neuroglia/patologia , Transdução de Sinais/efeitos dos fármacos , Acidente Vascular Cerebral/patologia , Fator de Crescimento Transformador beta1/farmacologia , Animais , Astrócitos/citologia , Astrócitos/efeitos dos fármacos , Astrócitos/metabolismo , Células Cultivadas , Cicatriz/patologia , Modelos Animais de Doenças , Domínio de Fibronectina Tipo III/genética , Proteínas Ligadas por GPI , Masculino , Proteínas de Membrana/antagonistas & inibidores , Proteínas de Membrana/genética , Proteínas do Tecido Nervoso/antagonistas & inibidores , Proteínas do Tecido Nervoso/genética , Fosforilação , Interferência de RNA , RNA Interferente Pequeno/metabolismo , Ratos , Ratos Sprague-Dawley , Receptor do Fator de Crescimento Transformador beta Tipo I/metabolismo , Proteína Smad2/metabolismo , Proteína Smad3/metabolismo , Acidente Vascular Cerebral/metabolismo
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