دورية أكاديمية
أعرض في EDS

Inhibition of hypoxia-inducible factors suppresses subretinal fibrosis.

التفاصيل البيبلوغرافية
العنوان: Inhibition of hypoxia-inducible factors suppresses subretinal fibrosis.
المؤلفون: Shoda C; Laboratory of Photobiology, Keio University School of Medicine, Tokyo, Japan.; Ophthalmology, Keio University School of Medicine, Tokyo, Japan.; Ophthalmology, Nihon University School of Medicine, Tokyo, Japan., Lee D; Laboratory of Photobiology, Keio University School of Medicine, Tokyo, Japan.; Ophthalmology, Keio University School of Medicine, Tokyo, Japan., Miwa Y; Laboratory of Photobiology, Keio University School of Medicine, Tokyo, Japan.; Ophthalmology, Keio University School of Medicine, Tokyo, Japan.; Aichi Animal Eye Clinic, Nagoya, Aichi, Japan., Yamagami S; Ophthalmology, Nihon University School of Medicine, Tokyo, Japan., Nakashizuka H; Ophthalmology, Nihon University School of Medicine, Tokyo, Japan., Nimura K; Shizuoka Prefectural Research Institute of Fishery and Ocean, Shizuoka, Japan., Okamoto K; Shizuoka Prefectural Research Institute of Fishery and Ocean, Shizuoka, Japan.; Marine Open Innovation Institute, Shizuoka, Japan., Kawagishi H; Faculty of Agriculture, Shizuoka University, Shizuoka, Japan.; Research Institute for Mushroom Science, Shizuoka University, Shizuoka, Japan., Negishi K; Ophthalmology, Keio University School of Medicine, Tokyo, Japan., Kurihara T; Laboratory of Photobiology, Keio University School of Medicine, Tokyo, Japan.; Ophthalmology, Keio University School of Medicine, Tokyo, Japan.
المصدر: FASEB journal : official publication of the Federation of American Societies for Experimental Biology [FASEB J] 2024 Jul 15; Vol. 38 (13), pp. e23792.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Federation of American Societies for Experimental Biology Country of Publication: United States NLM ID: 8804484 Publication Model: Print Cited Medium: Internet ISSN: 1530-6860 (Electronic) Linking ISSN: 08926638 NLM ISO Abbreviation: FASEB J Subsets: MEDLINE
أسماء مطبوعة: Publication: 2020- : [Bethesda, Md.] : Hoboken, NJ : Federation of American Societies for Experimental Biology ; Wiley
Original Publication: [Bethesda, Md.] : The Federation, [c1987-
مواضيع طبية MeSH: Fibrosis*/metabolism , Retinal Pigment Epithelium*/metabolism , Retinal Pigment Epithelium*/pathology , Von Hippel-Lindau Tumor Suppressor Protein*/metabolism , Von Hippel-Lindau Tumor Suppressor Protein*/genetics , Mice, Knockout*, Animals ; Mice ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics ; Hypoxia-Inducible Factor 1, alpha Subunit/antagonists & inhibitors ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Basic Helix-Loop-Helix Transcription Factors/antagonists & inhibitors ; Macular Degeneration/metabolism ; Macular Degeneration/pathology ; Macular Degeneration/drug therapy ; Retina/metabolism ; Retina/pathology ; Epithelial-Mesenchymal Transition/drug effects ; Mice, Inbred C57BL
مستخلص: Age-related macular degeneration (AMD) is a common cause of vision loss. The aggressive form of AMD is associated with ocular neovascularization and subretinal fibrosis, representing a responsive outcome against neovascularization mediated by epithelial-mesenchymal transition of retinal pigment epithelium (RPE) cells. A failure of the current treatment (anti-vascular endothelial growth factor therapy) has also been attributed to the progression of subretinal fibrosis. Hypoxia-inducible factors (HIFs) increase gene expressions to promote fibrosis and neovascularization. HIFs act as a central pathway in the pathogenesis of AMD. HIF inhibitors may suppress ocular neovascularization. Nonetheless, further investigation is required to unravel the aspects of subretinal fibrosis. In this study, we used RPE-specific HIFs or von Hippel-Lindau (VHL, a regulator of HIFs) conditional knockout (cKO) mice, along with pharmacological HIF inhibitors, to demonstrate the suppression of subretinal fibrosis. Fibrosis was suppressed by treatments of HIF inhibitors, and similar suppressive effects were detected in RPE-specific Hif1a/Hif2a- and Hif1a-cKO mice. Promotive effects were observed in RPE-specific Vhl-cKO mice, where fibrosis-mediated pathologic processes were evident. Marine products' extracts and their component taurine suppressed fibrosis as HIF inhibitors. Our study shows critical roles of HIFs in the progression of fibrosis, linking them to the potential development of therapeutics for AMD.
(© 2024 The Author(s). The FASEB Journal published by Wiley Periodicals LLC on behalf of Federation of American Societies for Experimental Biology.)
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معلومات مُعتمدة: 18K09424 KAKENHI; 24K12770 KAKENHI; Development of Research Seeds Based on Marine Biotechnology from Shizuoka Prefecture; JPMJSP2123 JST SPRING; JP22gm1510007 AMED
فهرسة مساهمة: Keywords: age‐related macular degeneration; choroidal neovascularization; hypoxia‐inducible factors; macular neovascularization; retinal pigment epithelium; subretinal fibrosis
المشرفين على المادة: EC 2.3.2.27 (Von Hippel-Lindau Tumor Suppressor Protein)
0 (Hypoxia-Inducible Factor 1, alpha Subunit)
0 (Basic Helix-Loop-Helix Transcription Factors)
0 (Hif1a protein, mouse)
EC 6.3.2.- (VHL protein, mouse)
1B37H0967P (endothelial PAS domain-containing protein 1)
تواريخ الأحداث: Date Created: 20240702 Date Completed: 20240702 Latest Revision: 20240702
رمز التحديث: 20240703
DOI: 10.1096/fj.202400540RRR
PMID: 38953555
قاعدة البيانات: MEDLINE
الوصف
تدمد:1530-6860
DOI:10.1096/fj.202400540RRR