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Available Therapeutic Options for Corneal Neovascularization: A Review
Corneal neovascularization can impair vision and result in a poor quality of life. The pathogenesis involves a complex interplay of angiogenic factors, notably vascular endothelial growth factor (VEGF). This review provides a comprehensive overview of potential therapies for corneal neovascularizati...
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Published in: | International journal of molecular sciences 2024-05, Vol.25 (10), p.5479 |
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description | Corneal neovascularization can impair vision and result in a poor quality of life. The pathogenesis involves a complex interplay of angiogenic factors, notably vascular endothelial growth factor (VEGF). This review provides a comprehensive overview of potential therapies for corneal neovascularization, covering tissue inhibitors of metalloproteinases (TIMPs), transforming growth factor beta (TGF-β) inhibitors, interleukin-1L receptor antagonist (IL-1 Ra), nitric oxide synthase (NOS) isoforms, galectin-3 inhibitors, retinal pigment epithelium-derived factor (PEDF), platelet-derived growth factor (PDGF) receptor inhibitors, and surgical treatments. Conventional treatments include anti-VEGF therapy and laser interventions, while emerging therapies such as immunosuppressive drugs (cyclosporine and rapamycin) have been explored. Losartan and decorin are potential antifibrotic agents that mitigate TGF-β-induced fibrosis. Ocular nanosystems are innovative drug-delivery platforms that facilitate the targeted release of therapeutic agents. Gene therapies, such as small interfering RNA and antisense oligonucleotides, are promising approaches for selectively inhibiting angiogenesis-related gene expression. Aganirsen is efficacious in reducing the corneal neovascularization area without significant adverse effects. These multifaceted approaches underscore the corneal neovascularization management complexity and highlight ideas for enhancing therapeutic outcomes. Furthermore, the importance of combination therapies and the need for further research to develop specific inhibitors while considering their therapeutic efficacy and potential adverse effects are discussed. |
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The pathogenesis involves a complex interplay of angiogenic factors, notably vascular endothelial growth factor (VEGF). This review provides a comprehensive overview of potential therapies for corneal neovascularization, covering tissue inhibitors of metalloproteinases (TIMPs), transforming growth factor beta (TGF-β) inhibitors, interleukin-1L receptor antagonist (IL-1 Ra), nitric oxide synthase (NOS) isoforms, galectin-3 inhibitors, retinal pigment epithelium-derived factor (PEDF), platelet-derived growth factor (PDGF) receptor inhibitors, and surgical treatments. Conventional treatments include anti-VEGF therapy and laser interventions, while emerging therapies such as immunosuppressive drugs (cyclosporine and rapamycin) have been explored. Losartan and decorin are potential antifibrotic agents that mitigate TGF-β-induced fibrosis. Ocular nanosystems are innovative drug-delivery platforms that facilitate the targeted release of therapeutic agents. Gene therapies, such as small interfering RNA and antisense oligonucleotides, are promising approaches for selectively inhibiting angiogenesis-related gene expression. Aganirsen is efficacious in reducing the corneal neovascularization area without significant adverse effects. These multifaceted approaches underscore the corneal neovascularization management complexity and highlight ideas for enhancing therapeutic outcomes. Furthermore, the importance of combination therapies and the need for further research to develop specific inhibitors while considering their therapeutic efficacy and potential adverse effects are discussed.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms25105479</identifier><identifier>PMID: 38791518</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Adapter proteins ; Angiogenesis ; Angiogenesis Inhibitors - therapeutic use ; angiogenic factors ; Animals ; antiangiogenic factors ; Blood vessels ; Bromfenac ; Cell adhesion & migration ; Cell growth ; Cornea ; Corneal Neovascularization - drug therapy ; Corneal Neovascularization - metabolism ; Corneal Neovascularization - therapy ; Cytokines ; Difluprednate ; Edema ; Endothelium ; Enzymes ; Extracellular matrix ; Fibroblasts ; Gene expression ; Genetic Therapy - methods ; Growth factors ; Health aspects ; Heparan sulfate ; Humans ; Hypoxia ; Inflammation ; Interleukins ; Kinases ; Ligands ; Lipids ; Neovascularization ; Nepafenac ; Nitric oxide ; nonsteroidal anti-inflammatory drugs ; Permeability ; Physiology ; steroids ; Transforming Growth Factor beta - metabolism ; Tumor necrosis factor-TNF ; Vascular endothelial growth factor</subject><ispartof>International journal of molecular sciences, 2024-05, Vol.25 (10), p.5479</ispartof><rights>COPYRIGHT 2024 MDPI AG</rights><rights>2024 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). 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Gene therapies, such as small interfering RNA and antisense oligonucleotides, are promising approaches for selectively inhibiting angiogenesis-related gene expression. Aganirsen is efficacious in reducing the corneal neovascularization area without significant adverse effects. These multifaceted approaches underscore the corneal neovascularization management complexity and highlight ideas for enhancing therapeutic outcomes. Furthermore, the importance of combination therapies and the need for further research to develop specific inhibitors while considering their therapeutic efficacy and potential adverse effects are discussed.</description><subject>Adapter proteins</subject><subject>Angiogenesis</subject><subject>Angiogenesis Inhibitors - therapeutic use</subject><subject>angiogenic factors</subject><subject>Animals</subject><subject>antiangiogenic factors</subject><subject>Blood vessels</subject><subject>Bromfenac</subject><subject>Cell adhesion & migration</subject><subject>Cell growth</subject><subject>Cornea</subject><subject>Corneal Neovascularization - drug therapy</subject><subject>Corneal Neovascularization - metabolism</subject><subject>Corneal Neovascularization - therapy</subject><subject>Cytokines</subject><subject>Difluprednate</subject><subject>Edema</subject><subject>Endothelium</subject><subject>Enzymes</subject><subject>Extracellular matrix</subject><subject>Fibroblasts</subject><subject>Gene expression</subject><subject>Genetic Therapy - methods</subject><subject>Growth factors</subject><subject>Health aspects</subject><subject>Heparan sulfate</subject><subject>Humans</subject><subject>Hypoxia</subject><subject>Inflammation</subject><subject>Interleukins</subject><subject>Kinases</subject><subject>Ligands</subject><subject>Lipids</subject><subject>Neovascularization</subject><subject>Nepafenac</subject><subject>Nitric oxide</subject><subject>nonsteroidal anti-inflammatory drugs</subject><subject>Permeability</subject><subject>Physiology</subject><subject>steroids</subject><subject>Transforming Growth Factor beta - metabolism</subject><subject>Tumor necrosis factor-TNF</subject><subject>Vascular endothelial growth factor</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNptkkFvEzEQhS0EoiVw44xW4sKBFNtjr9fcoqiFShWVUDlbs85scbRZB3s3CH59naZUASEfbM1882aePIy9FvwMwPIPYb3JUguulbFP2KlQUs45r83To_cJe5HzmnMJUtvn7AQaY4UWzSm7WOww9Nj2VN18p4Rbmsbgq-vtGOKQqy6mahnTQNhXXyjuMPupxxR-4z7_sVpUX2kX6OdL9qzDPtOrh3vGvl2c3yw_z6-uP10uF1dzr5QZ5yQt1jUHX8aVvKHOKuAIUoFQnZAI5DmggFYYDahRt-2KJFnDPaEBCTN2edBdRVy7bQobTL9cxODuAzHdOkzFQE-usR2KuvXAqVGlW-ttrQwZz73k-l7r3UFrm-KPifLoNiF76nscKE7ZAS-TNqC4Kujbf9B1nNJQnBZKFxMC9BF1i6V_GLo4JvR7UbcwVoMVvDSesbP_UOWsaBN8HKgLJf5XwftDgU8x50Tdo2_B3X4F3PEKFPzNw6xTu6HVI_znz-EOjiqoAQ</recordid><startdate>20240501</startdate><enddate>20240501</enddate><creator>Drzyzga, Łukasz</creator><creator>Śpiewak, Dorota</creator><creator>Dorecka, Mariola</creator><creator>Wyględowska-Promieńska, Dorota</creator><general>MDPI AG</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>DOA</scope><orcidid>https://orcid.org/0009-0001-3596-7970</orcidid></search><sort><creationdate>20240501</creationdate><title>Available Therapeutic Options for Corneal Neovascularization: A Review</title><author>Drzyzga, Łukasz ; 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The pathogenesis involves a complex interplay of angiogenic factors, notably vascular endothelial growth factor (VEGF). This review provides a comprehensive overview of potential therapies for corneal neovascularization, covering tissue inhibitors of metalloproteinases (TIMPs), transforming growth factor beta (TGF-β) inhibitors, interleukin-1L receptor antagonist (IL-1 Ra), nitric oxide synthase (NOS) isoforms, galectin-3 inhibitors, retinal pigment epithelium-derived factor (PEDF), platelet-derived growth factor (PDGF) receptor inhibitors, and surgical treatments. Conventional treatments include anti-VEGF therapy and laser interventions, while emerging therapies such as immunosuppressive drugs (cyclosporine and rapamycin) have been explored. Losartan and decorin are potential antifibrotic agents that mitigate TGF-β-induced fibrosis. Ocular nanosystems are innovative drug-delivery platforms that facilitate the targeted release of therapeutic agents. Gene therapies, such as small interfering RNA and antisense oligonucleotides, are promising approaches for selectively inhibiting angiogenesis-related gene expression. Aganirsen is efficacious in reducing the corneal neovascularization area without significant adverse effects. These multifaceted approaches underscore the corneal neovascularization management complexity and highlight ideas for enhancing therapeutic outcomes. Furthermore, the importance of combination therapies and the need for further research to develop specific inhibitors while considering their therapeutic efficacy and potential adverse effects are discussed.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>38791518</pmid><doi>10.3390/ijms25105479</doi><orcidid>https://orcid.org/0009-0001-3596-7970</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Adapter proteins Angiogenesis Angiogenesis Inhibitors - therapeutic use angiogenic factors Animals antiangiogenic factors Blood vessels Bromfenac Cell adhesion & migration Cell growth Cornea Corneal Neovascularization - drug therapy Corneal Neovascularization - metabolism Corneal Neovascularization - therapy Cytokines Difluprednate Edema Endothelium Enzymes Extracellular matrix Fibroblasts Gene expression Genetic Therapy - methods Growth factors Health aspects Heparan sulfate Humans Hypoxia Inflammation Interleukins Kinases Ligands Lipids Neovascularization Nepafenac Nitric oxide nonsteroidal anti-inflammatory drugs Permeability Physiology steroids Transforming Growth Factor beta - metabolism Tumor necrosis factor-TNF Vascular endothelial growth factor |
title | Available Therapeutic Options for Corneal Neovascularization: A Review |
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