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Subretinal fibrosis secondary to neovascular age-related macular degeneration:mechanisms and potential therapeutic targets

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Neural Regeneration Research 2025年第2期20卷 378-393页

作者： Jingxiang Zhang Xia Sheng Quanju Ding Yujun Wang Jiwei Zhao Jingfa Zhang Department of Ophthalmology People’s Hospital of Huangdao DistrictQingdaoShandong ProvinceChina Department of Urology People’s Hospital of Huangdao DistrictQingdaoShandong ProvinceChina Department of Ophthalmology Shanghai General Hospital(Shanghai First People’s Hospital)Shanghai Jiao Tong University School of MedicineShanghaiChina National Clinical Research Center for Eye Diseases Shanghai Key Laboratory of Ocular Fundus DiseasesShanghai Engineering Center for Visual Science and PhotomedicineShanghai Engineering Center for Precise Diagnosis and Treatment of Eye DiseasesShanghaiChina

Subretinal fibrosis is the end-stage sequelae of neovascular age-related macular *** causes local damage to photoreceptors,retinal pigment epithelium,and choroidal vessels,which leads to permanent central vision loss of patients with neovascular age-related macular *** pathogenesis of subretinal fibrosis is complex,and the underlying mechanisms are largely ***,there are no effective treatment options.A thorough understanding of the pathogenesis of subretinal fibrosis and its related mechanisms is important to elucidate its complications and explore potential *** current article reviews several aspects of subretinal fibrosis,including the current understanding on the relationship between neovascular age-related macular degeneration and subretinal fibrosis;multimodal imaging techniques for subretinal fibrosis;animal models for studying subretinal fibrosis;cellular and non-cellular constituents of subretinal fibrosis;pathophysiological mechanisms involved in subretinal fibrosis,such as aging,infiltration of macrophages,different sources of mesenchymal transition to myofibroblast,and activation of complement system and immune cells;and several key molecules and signaling pathways participating in the pathogenesis of subretinal fibrosis,such as vascular endothelial growth factor,connective tissue growth factor,fibroblast growth factor 2,platelet-derived growth factor and platelet-derived growth factor receptor-β,transforming growth factor-βsignaling pathway,Wnt signaling pathway,and the axis of heat shock protein 70-Toll-like receptors 2/*** review will improve the understanding of the pathogenesis of subretinal fibrosis,allow the discovery of molecular targets,and explore potential treatments for the management of subretinal fibrosis.

关键词： choroidal neovascularization epithelial-mesenchymal transition mesenchymal transition myofibroblast neovascular age-related macular degeneration submacular fibrosis subretinal fibrosis therapeutic targets transforming growth factor-β vascular endothelial growth factor

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Comprehensive understanding of glioblastoma molecular phenotypes:classification,characteristics,and transition

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Cancer Biology & Medicine 2024年第5期21卷 363-381页

作者： Can Xu Pengyu Hou Xiang Li Menglin Xiao Ziqi Zhang Ziru Li Jianglong Xu Guoming Liu Yanli Tan Chuan Fang School of Clinical Medicine Hebei UniversityDepartment of NeurosurgeryAffiliated Hospital of Hebei UniversityBaoding 07100China Hebei Key Laboratory of Precise Diagnosis and Treatment of Glioma Baoding 071000China School of Basic Medical Sciences Hebei UniversityBaoding 07100China Department of Pathology Affiliated Hospital of Hebei UniversityBaoding 07100China

Among central nervous system-associated malignancies,glioblastoma(GBM)is the most common and has the highest mortality *** high heterogeneity of GBM cell types and the complex tumor microenvironment frequently lead to tumor recurrence and sudden relapse in patients treated with *** precision medicine,research on GBM treatment is increasingly focusing on molecular subtyping to precisely characterize the cellular and molecular heterogeneity,as well as the refractory nature of GBM toward *** understanding of the different molecular expression patterns of GBM subtypes is *** have recently proposed tetra fractional or tripartite methods for detecting GBM molecular *** various molecular subtypes of GBM show significant differences in gene expression patterns and biological *** subtypes also exhibit high plasticity in their regulatory pathways,oncogene expression,tumor microenvironment alterations,and differential responses to standard ***,we summarize the current molecular typing scheme of GBM and the major molecular/genetic characteristics of each ***,we review the mesenchymal transition mechanisms of GBM under various regulators.

关键词： Glioblastoma molecular phenotype classification characteristic mesenchymal transition

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Aldosterone-induced mesangial cell proliferation is mediated by EGF receptor transactivation

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南京医科大学学报(自然科学版) 2009年第7期 991-991页

作者： Huang, S. M. Zhang, A. H. Ding, G. X. Chen, R. H. Nanjing Med Univ, Nanjing Childrens Hosp, Dept Nephrol, Nanjing, Peoples R China. Nanjing Med Univ, Inst Pediat, Nanjing, Peoples R China.

Huang S, Zhang A, Ding G, Chen R. Aldosterone-induced mesangial cell proliferation is mediated by EGF receptor transactivation. Am J Physiol Renal Physiol 296: F1323-F1333, 2009. First published April 1, 2009; doi: 10.1152 / ajprenal. 90428.2008. -Aldosterone (Aldo) stimulates glomerular mesangial cell (MC) proliferation, in part, through an ERK1 / 2-dependent pathway. In this study, we examined whether Aldo activation of ERK1 / 2 in MC is mediated through redox-dependent EGF receptor (EGFR) transactivation, as well as the involvement of other signaling mechanisms in Aldo-induced MC proliferation. Aldo increased human MC proliferation, as determined by [H-3]thymidine incorporation and cell counts. This increase in proliferation was blocked by inhibition of the mineralocorticoid receptor (MR). Continuing our observations downstream in the signaling pathway, we examined the ability of Aldo to activate both the Ras / MAPK and the PI3K signaling pathways. Aldo increased Ki-RasA and Ki-RasA:GTP levels, and sequentially phosphorylated c-Raf, MAPK kinase (MEK1 / 2), and ERK1 / 2. Ki-RasA small interfering RNA (siRNA), the c-Raf inhibitor GW5074, and the MEK1 / 2 inhibitor PD98059 reduced Aldo-induced cell proliferation by similar to 65%. Aldo also increased phosphorylation of PI3K, Akt, the mammalian target of rapamycin (mTOR), and the 70-kDa ribosomal S6 kinase (p70S6K1). Inhibition of the PI3K pathways by the selective PI3K inhibitor LY 294002, an Akt inhibitor, or the mTOR inhibitor rapamycin reduced cell proliferation by 51% . Combining LY 294002 and PD98059 completely blocked Aldo-induced MC proliferation. Next, we confirmed that Aldo exerts its effect on MAPK and PI3K activation, as well as on cell proliferation, by activating the EGFR. Pretreatment with the EGFR antagonist AG1478 inhibited MC proliferation, as well as the activation of Ras / MAPK and PI3K / Akt, suggesting that Ras / MAPK and PI3K / Akt activation occur downstream of EGFR activation. Finally, we exa

关键词： reactive oxygen species PI3K hypertensive-rats phosphatidylinositol 3-kinase stimulates proliferation mesenchymal transition epithelial-cells nadph oxidase s6 kinase activation ras cascade

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