The molecular mechanisms of action of PPAR-γ agonists in the treatment of corneal alkali burns (Review)
Corneal alkali burns (CAB) are characterized by injury-induced inflammation, fibrosis and neovascularization (NV), and may lead to blindness. This review evaluates the current knowledge of the molecular mechanisms responsible for CAB. The processes of cytokine production, chemotaxis, inflammatory re...
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| Veröffentlicht in: | International journal of molecular medicine 2016-10, Vol.38 (4), p.1003-1011 |
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| creator | Zhou, Hongyan Zhang, Wensong Bi, Miaomiao Wu, Jie |
| description | Corneal alkali burns (CAB) are characterized by injury-induced inflammation, fibrosis and neovascularization (NV), and may lead to blindness. This review evaluates the current knowledge of the molecular mechanisms responsible for CAB. The processes of cytokine production, chemotaxis, inflammatory responses, immune response, cell signal transduction, matrix metalloproteinase production and vascular factors in CAB are discussed. Previous evidence indicates that peroxisome proliferator-activated receptor γ (PPAR-γ) agonists suppress immune responses, inflammation, corneal fibrosis and NV. This review also discusses the role of PPAR-γ as an anti-inflammatory, anti-fibrotic and anti-angiogenic agent in the treatment of CAB, as well as the potential role of PPAR-γ in the pathological process of CAB. There have been numerous studies evaluating the clinical profiles of CAB, and the aim of this systematic review was to summarize the evidence regarding the treatment of CAB with PPAR-γ agonists. |
| doi_str_mv | 10.3892/ijmm.2016.2699 |
| format | Article |
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This review evaluates the current knowledge of the molecular mechanisms responsible for CAB. The processes of cytokine production, chemotaxis, inflammatory responses, immune response, cell signal transduction, matrix metalloproteinase production and vascular factors in CAB are discussed. Previous evidence indicates that peroxisome proliferator-activated receptor γ (PPAR-γ) agonists suppress immune responses, inflammation, corneal fibrosis and NV. This review also discusses the role of PPAR-γ as an anti-inflammatory, anti-fibrotic and anti-angiogenic agent in the treatment of CAB, as well as the potential role of PPAR-γ in the pathological process of CAB. There have been numerous studies evaluating the clinical profiles of CAB, and the aim of this systematic review was to summarize the evidence regarding the treatment of CAB with PPAR-γ agonists.</description><identifier>ISSN: 1107-3756</identifier><identifier>EISSN: 1791-244X</identifier><identifier>DOI: 10.3892/ijmm.2016.2699</identifier><identifier>PMID: 27499172</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>agonists ; Alkalies ; Angiogenesis ; Atherosclerosis ; Burns ; Burns, Chemical ; Care and treatment ; Cell adhesion & migration ; Chemokines ; Complications and side effects ; Cornea ; Cornea - pathology ; corneal alkali burn ; corneal neovascularization ; Cytokines ; Eye Burns - drug therapy ; Eye Burns - metabolism ; Gene expression ; Genetic aspects ; Humans ; Immune response ; Inflammation ; Injuries ; Kinases ; Ligands ; Observations ; peroxisome proliferator-activated receptor-γ ; PPAR gamma - agonists ; PPAR gamma - metabolism ; Proteins ; Risk factors ; Scars ; Signal transduction ; Stem cells ; Studies ; Translational Medical Research ; Tumor necrosis factor-TNF ; Vascular endothelial growth factor ; Wound Healing</subject><ispartof>International journal of molecular medicine, 2016-10, Vol.38 (4), p.1003-1011</ispartof><rights>Copyright: © Zhou et al.</rights><rights>COPYRIGHT 2016 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2016</rights><rights>Copyright: © Zhou et al. 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c448t-13a9f37c6e5d240225df37839cbabd128eaffab108576f58c0bf2a2026d584263</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,5571,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27499172$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhou, Hongyan</creatorcontrib><creatorcontrib>Zhang, Wensong</creatorcontrib><creatorcontrib>Bi, Miaomiao</creatorcontrib><creatorcontrib>Wu, Jie</creatorcontrib><title>The molecular mechanisms of action of PPAR-γ agonists in the treatment of corneal alkali burns (Review)</title><title>International journal of molecular medicine</title><addtitle>Int J Mol Med</addtitle><description>Corneal alkali burns (CAB) are characterized by injury-induced inflammation, fibrosis and neovascularization (NV), and may lead to blindness. This review evaluates the current knowledge of the molecular mechanisms responsible for CAB. The processes of cytokine production, chemotaxis, inflammatory responses, immune response, cell signal transduction, matrix metalloproteinase production and vascular factors in CAB are discussed. Previous evidence indicates that peroxisome proliferator-activated receptor γ (PPAR-γ) agonists suppress immune responses, inflammation, corneal fibrosis and NV. This review also discusses the role of PPAR-γ as an anti-inflammatory, anti-fibrotic and anti-angiogenic agent in the treatment of CAB, as well as the potential role of PPAR-γ in the pathological process of CAB. There have been numerous studies evaluating the clinical profiles of CAB, and the aim of this systematic review was to summarize the evidence regarding the treatment of CAB with PPAR-γ agonists.</description><subject>agonists</subject><subject>Alkalies</subject><subject>Angiogenesis</subject><subject>Atherosclerosis</subject><subject>Burns</subject><subject>Burns, Chemical</subject><subject>Care and treatment</subject><subject>Cell adhesion & migration</subject><subject>Chemokines</subject><subject>Complications and side effects</subject><subject>Cornea</subject><subject>Cornea - pathology</subject><subject>corneal alkali burn</subject><subject>corneal neovascularization</subject><subject>Cytokines</subject><subject>Eye Burns - drug therapy</subject><subject>Eye Burns - metabolism</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Humans</subject><subject>Immune response</subject><subject>Inflammation</subject><subject>Injuries</subject><subject>Kinases</subject><subject>Ligands</subject><subject>Observations</subject><subject>peroxisome proliferator-activated receptor-γ</subject><subject>PPAR gamma - agonists</subject><subject>PPAR gamma - metabolism</subject><subject>Proteins</subject><subject>Risk factors</subject><subject>Scars</subject><subject>Signal transduction</subject><subject>Stem cells</subject><subject>Studies</subject><subject>Translational Medical Research</subject><subject>Tumor necrosis factor-TNF</subject><subject>Vascular endothelial growth factor</subject><subject>Wound Healing</subject><issn>1107-3756</issn><issn>1791-244X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkc9qFTEUxgdRbK1uXUrATV3MNTnJZJKNcCn-g4KlVHAXMpnk3lwnSU3mVnwu38NnMkPrVaFkkZOc3_dxDl_TPCd4RYWE134Xwgow4SvgUj5ojkkvSQuMfXlYa4L7lvYdP2qelLLDGDomxePmCHomJenhuNlebS0KabJmP-mMgjVbHX0JBSWHtJl9ikt1cbG-bH_9RHqTancuyEc0V-WcrZ6DjfMCmZSj1RPS01c9eTTscyzo9NLeePv91dPmkdNTsc_u7pPm87u3V2cf2vNP7z-erc9bw5iYW0K1dLQ33HYjMAzQjfUpqDSDHkYCwmrn9ECw6HruOmHw4EADBj52ggGnJ82bW9_r_RDsaOpsWU_qOvug8w-VtFf_d6Lfqk26UR0GKTmtBi_vDHL6trdlVrtUN6kzKyIpUJDAyF9qoyerfHSpmpngi1FrxrlgnLK-Uqt7qHpGG7xJ0Tpf_-8TmJxKydYdBidYLYGrJXC1BK6WwKvgxb_rHvA_CVfg9BYo1zqOfkzlwCxWLRUtZi3BmNLfMxK0yQ</recordid><startdate>20161001</startdate><enddate>20161001</enddate><creator>Zhou, Hongyan</creator><creator>Zhang, Wensong</creator><creator>Bi, Miaomiao</creator><creator>Wu, Jie</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</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>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope></search><sort><creationdate>20161001</creationdate><title>The molecular mechanisms of action of PPAR-γ agonists in the treatment of corneal alkali burns (Review)</title><author>Zhou, Hongyan ; Zhang, Wensong ; Bi, Miaomiao ; Wu, Jie</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c448t-13a9f37c6e5d240225df37839cbabd128eaffab108576f58c0bf2a2026d584263</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>agonists</topic><topic>Alkalies</topic><topic>Angiogenesis</topic><topic>Atherosclerosis</topic><topic>Burns</topic><topic>Burns, Chemical</topic><topic>Care and treatment</topic><topic>Cell adhesion & migration</topic><topic>Chemokines</topic><topic>Complications and side effects</topic><topic>Cornea</topic><topic>Cornea - pathology</topic><topic>corneal alkali burn</topic><topic>corneal neovascularization</topic><topic>Cytokines</topic><topic>Eye Burns - drug therapy</topic><topic>Eye Burns - metabolism</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Humans</topic><topic>Immune response</topic><topic>Inflammation</topic><topic>Injuries</topic><topic>Kinases</topic><topic>Ligands</topic><topic>Observations</topic><topic>peroxisome proliferator-activated receptor-γ</topic><topic>PPAR gamma - agonists</topic><topic>PPAR gamma - metabolism</topic><topic>Proteins</topic><topic>Risk factors</topic><topic>Scars</topic><topic>Signal transduction</topic><topic>Stem cells</topic><topic>Studies</topic><topic>Translational Medical Research</topic><topic>Tumor necrosis factor-TNF</topic><topic>Vascular endothelial growth factor</topic><topic>Wound Healing</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhou, Hongyan</creatorcontrib><creatorcontrib>Zhang, Wensong</creatorcontrib><creatorcontrib>Bi, Miaomiao</creatorcontrib><creatorcontrib>Wu, Jie</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhou, Hongyan</au><au>Zhang, Wensong</au><au>Bi, Miaomiao</au><au>Wu, Jie</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The molecular mechanisms of action of PPAR-γ agonists in the treatment of corneal alkali burns (Review)</atitle><jtitle>International journal of molecular medicine</jtitle><addtitle>Int J Mol Med</addtitle><date>2016-10-01</date><risdate>2016</risdate><volume>38</volume><issue>4</issue><spage>1003</spage><epage>1011</epage><pages>1003-1011</pages><issn>1107-3756</issn><eissn>1791-244X</eissn><abstract>Corneal alkali burns (CAB) are characterized by injury-induced inflammation, fibrosis and neovascularization (NV), and may lead to blindness. This review evaluates the current knowledge of the molecular mechanisms responsible for CAB. The processes of cytokine production, chemotaxis, inflammatory responses, immune response, cell signal transduction, matrix metalloproteinase production and vascular factors in CAB are discussed. Previous evidence indicates that peroxisome proliferator-activated receptor γ (PPAR-γ) agonists suppress immune responses, inflammation, corneal fibrosis and NV. This review also discusses the role of PPAR-γ as an anti-inflammatory, anti-fibrotic and anti-angiogenic agent in the treatment of CAB, as well as the potential role of PPAR-γ in the pathological process of CAB. There have been numerous studies evaluating the clinical profiles of CAB, and the aim of this systematic review was to summarize the evidence regarding the treatment of CAB with PPAR-γ agonists.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>27499172</pmid><doi>10.3892/ijmm.2016.2699</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | agonists Alkalies Angiogenesis Atherosclerosis Burns Burns, Chemical Care and treatment Cell adhesion & migration Chemokines Complications and side effects Cornea Cornea - pathology corneal alkali burn corneal neovascularization Cytokines Eye Burns - drug therapy Eye Burns - metabolism Gene expression Genetic aspects Humans Immune response Inflammation Injuries Kinases Ligands Observations peroxisome proliferator-activated receptor-γ PPAR gamma - agonists PPAR gamma - metabolism Proteins Risk factors Scars Signal transduction Stem cells Studies Translational Medical Research Tumor necrosis factor-TNF Vascular endothelial growth factor Wound Healing |
| title | The molecular mechanisms of action of PPAR-γ agonists in the treatment of corneal alkali burns (Review) |
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