Insulin-Like Growth Factor-1 Signaling in Lung Development and Inflammatory Lung Diseases
Insulin-like growth factor-1 (IGF-1) was firstly identified as a hormone that mediates the biological effects of growth hormone. Accumulating data have indicated the role of IGF-1 signaling pathway in lung development and diseases such as congenital disorders, cancers, inflammation, and fibrosis. IG...
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description | Insulin-like growth factor-1 (IGF-1) was firstly identified as a hormone that mediates the biological effects of growth hormone. Accumulating data have indicated the role of IGF-1 signaling pathway in lung development and diseases such as congenital disorders, cancers, inflammation, and fibrosis. IGF-1 signaling modulates the development and differentiation of many types of lung cells, including airway basal cells, club cells, alveolar epithelial cells, and fibroblasts. IGF-1 signaling deficiency results in alveolar hyperplasia in humans and disrupted lung architecture in animal models. The components of IGF-1 signaling pathways are potentiated as biomarkers as they are dysregulated locally or systemically in lung diseases, whereas data may be inconsistent or even paradoxical among different studies. The usage of IGF-1-based therapeutic agents urges for more researches in developmental disorders and inflammatory lung diseases, as the majority of current data are collected from limited number of animal experiments and are generally less exuberant than those in lung cancer. Elucidation of these questions by further bench-to-bedside researches may provide us with rational clinical diagnostic approaches and agents concerning IGF-1 signaling in lung diseases. |
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Accumulating data have indicated the role of IGF-1 signaling pathway in lung development and diseases such as congenital disorders, cancers, inflammation, and fibrosis. IGF-1 signaling modulates the development and differentiation of many types of lung cells, including airway basal cells, club cells, alveolar epithelial cells, and fibroblasts. IGF-1 signaling deficiency results in alveolar hyperplasia in humans and disrupted lung architecture in animal models. The components of IGF-1 signaling pathways are potentiated as biomarkers as they are dysregulated locally or systemically in lung diseases, whereas data may be inconsistent or even paradoxical among different studies. The usage of IGF-1-based therapeutic agents urges for more researches in developmental disorders and inflammatory lung diseases, as the majority of current data are collected from limited number of animal experiments and are generally less exuberant than those in lung cancer. Elucidation of these questions by further bench-to-bedside researches may provide us with rational clinical diagnostic approaches and agents concerning IGF-1 signaling in lung diseases.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2018/6057589</identifier><identifier>PMID: 30018981</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Alveoli ; Animal experimentation ; Animal models ; Animal research ; Animals ; Apoptosis ; Basal cells ; Bioindicators ; Biological effects ; Biomarkers ; Cancer therapies ; Cell adhesion & migration ; Cell cycle ; Chemical compounds ; Congenital diseases ; Cystic fibrosis ; Development and progression ; Developmental disabilities ; Diagnostic systems ; Diseases ; Disorders ; Endocrinology ; Epithelial cells ; Fibroblasts ; Fibrosis ; Growth Hormone ; Growth hormones ; Humans ; Hyperplasia ; Inflammation ; Inflammatory diseases ; Insulin ; Insulin-like growth factor I ; Insulin-Like Growth Factor I - physiology ; Insulin-like growth factors ; Kinases ; Ligands ; Lung - growth & development ; Lung - pathology ; Lung cancer ; Lung diseases ; Lung Diseases - immunology ; Lung Neoplasms ; Medical research ; Medicine, Experimental ; Metabolism ; Pediatrics ; Peptides ; Pharmacology ; Phosphorylation ; Proteins ; Pulmonary arteries ; Respiratory tract ; Review ; Signal Transduction ; Signaling ; Somatotropin</subject><ispartof>BioMed research international, 2018-01, Vol.2018 (2018), p.1-27</ispartof><rights>Copyright © 2018 Zheng Wang et al.</rights><rights>COPYRIGHT 2018 John Wiley & Sons, Inc.</rights><rights>Copyright © 2018 Zheng Wang et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2018 Zheng Wang et al. 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c565t-a65ef96775e9829de6858721fa897d94c07a25b8fbd5733b476af4b9294c3fa23</citedby><cites>FETCH-LOGICAL-c565t-a65ef96775e9829de6858721fa897d94c07a25b8fbd5733b476af4b9294c3fa23</cites><orcidid>0000-0002-5189-0993 ; 0000-0001-7734-4838 ; 0000-0002-2833-8746</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6029485/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6029485/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30018981$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Siafakas, Nikolaos</contributor><creatorcontrib>Ma, Lijun</creatorcontrib><creatorcontrib>Wang, Yuming</creatorcontrib><creatorcontrib>Guo, Qiongya</creatorcontrib><creatorcontrib>Li, Wenting</creatorcontrib><creatorcontrib>Wang, Zheng</creatorcontrib><creatorcontrib>Zhang, Xiaoju</creatorcontrib><title>Insulin-Like Growth Factor-1 Signaling in Lung Development and Inflammatory Lung Diseases</title><title>BioMed research international</title><addtitle>Biomed Res Int</addtitle><description>Insulin-like growth factor-1 (IGF-1) was firstly identified as a hormone that mediates the biological effects of growth hormone. Accumulating data have indicated the role of IGF-1 signaling pathway in lung development and diseases such as congenital disorders, cancers, inflammation, and fibrosis. IGF-1 signaling modulates the development and differentiation of many types of lung cells, including airway basal cells, club cells, alveolar epithelial cells, and fibroblasts. IGF-1 signaling deficiency results in alveolar hyperplasia in humans and disrupted lung architecture in animal models. The components of IGF-1 signaling pathways are potentiated as biomarkers as they are dysregulated locally or systemically in lung diseases, whereas data may be inconsistent or even paradoxical among different studies. The usage of IGF-1-based therapeutic agents urges for more researches in developmental disorders and inflammatory lung diseases, as the majority of current data are collected from limited number of animal experiments and are generally less exuberant than those in lung cancer. Elucidation of these questions by further bench-to-bedside researches may provide us with rational clinical diagnostic approaches and agents concerning IGF-1 signaling in lung diseases.</description><subject>Alveoli</subject><subject>Animal experimentation</subject><subject>Animal models</subject><subject>Animal research</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Basal cells</subject><subject>Bioindicators</subject><subject>Biological effects</subject><subject>Biomarkers</subject><subject>Cancer therapies</subject><subject>Cell adhesion & migration</subject><subject>Cell cycle</subject><subject>Chemical compounds</subject><subject>Congenital diseases</subject><subject>Cystic fibrosis</subject><subject>Development and progression</subject><subject>Developmental disabilities</subject><subject>Diagnostic systems</subject><subject>Diseases</subject><subject>Disorders</subject><subject>Endocrinology</subject><subject>Epithelial cells</subject><subject>Fibroblasts</subject><subject>Fibrosis</subject><subject>Growth Hormone</subject><subject>Growth hormones</subject><subject>Humans</subject><subject>Hyperplasia</subject><subject>Inflammation</subject><subject>Inflammatory diseases</subject><subject>Insulin</subject><subject>Insulin-like growth factor I</subject><subject>Insulin-Like Growth Factor I - physiology</subject><subject>Insulin-like growth factors</subject><subject>Kinases</subject><subject>Ligands</subject><subject>Lung - growth & development</subject><subject>Lung - pathology</subject><subject>Lung cancer</subject><subject>Lung diseases</subject><subject>Lung Diseases - immunology</subject><subject>Lung Neoplasms</subject><subject>Medical research</subject><subject>Medicine, Experimental</subject><subject>Metabolism</subject><subject>Pediatrics</subject><subject>Peptides</subject><subject>Pharmacology</subject><subject>Phosphorylation</subject><subject>Proteins</subject><subject>Pulmonary arteries</subject><subject>Respiratory tract</subject><subject>Review</subject><subject>Signal Transduction</subject><subject>Signaling</subject><subject>Somatotropin</subject><issn>2314-6133</issn><issn>2314-6141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqNkc1v1DAQxSNERavSG2cUiQtSCfVH_HVBqgptV1qpB-DAyZok9q5LYi920qr_PY522Zae6stYej-_mfErincYfcaYsTOCsDzjiAkm1aviiFBcVxzX-PX-TulhcZLSLcpHYo4Uf1McUpTfKYmPil8Ln6be-WrpfpvyKob7cV1eQjuGWOHyu1t5yOqqdL5cTrl-NXemD5vB-LEE35ULb3sYBsj8w45wyUAy6W1xYKFP5mRXj4ufl99-XFxXy5urxcX5smoZZ2MFnBmruBDMKElUZ7hkUhBsQSrRqbpFAghrpG06JihtasHB1o0iWaIWCD0uvmx9N1MzmK7Nk0Xo9Sa6AeKDDuD0_4p3a70Kd5qj7CFZNvi4M4jhz2TSqAeXWtP34E2YkiZIYKY44TP64Rl6G6aYv2imOJFYCYEeqRX0RjtvQ-7bzqb6nBMsVG6rMvVpS7UxpBSN3Y-MkZ7D1XO4ehduxt8_XXMP_4syA6dbYO18B_fuhXYmM8bCI42JyGnQv_0TtBg</recordid><startdate>20180101</startdate><enddate>20180101</enddate><creator>Ma, Lijun</creator><creator>Wang, Yuming</creator><creator>Guo, Qiongya</creator><creator>Li, Wenting</creator><creator>Wang, Zheng</creator><creator>Zhang, Xiaoju</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><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>7QL</scope><scope>7QO</scope><scope>7T7</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>CWDGH</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-5189-0993</orcidid><orcidid>https://orcid.org/0000-0001-7734-4838</orcidid><orcidid>https://orcid.org/0000-0002-2833-8746</orcidid></search><sort><creationdate>20180101</creationdate><title>Insulin-Like Growth Factor-1 Signaling in Lung Development and Inflammatory Lung Diseases</title><author>Ma, Lijun ; Wang, Yuming ; Guo, Qiongya ; Li, Wenting ; Wang, Zheng ; Zhang, Xiaoju</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c565t-a65ef96775e9829de6858721fa897d94c07a25b8fbd5733b476af4b9294c3fa23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Alveoli</topic><topic>Animal experimentation</topic><topic>Animal models</topic><topic>Animal research</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Basal cells</topic><topic>Bioindicators</topic><topic>Biological effects</topic><topic>Biomarkers</topic><topic>Cancer therapies</topic><topic>Cell adhesion & migration</topic><topic>Cell cycle</topic><topic>Chemical compounds</topic><topic>Congenital diseases</topic><topic>Cystic fibrosis</topic><topic>Development and progression</topic><topic>Developmental disabilities</topic><topic>Diagnostic systems</topic><topic>Diseases</topic><topic>Disorders</topic><topic>Endocrinology</topic><topic>Epithelial cells</topic><topic>Fibroblasts</topic><topic>Fibrosis</topic><topic>Growth Hormone</topic><topic>Growth hormones</topic><topic>Humans</topic><topic>Hyperplasia</topic><topic>Inflammation</topic><topic>Inflammatory diseases</topic><topic>Insulin</topic><topic>Insulin-like growth factor I</topic><topic>Insulin-Like Growth Factor I - physiology</topic><topic>Insulin-like growth factors</topic><topic>Kinases</topic><topic>Ligands</topic><topic>Lung - growth & development</topic><topic>Lung - pathology</topic><topic>Lung cancer</topic><topic>Lung diseases</topic><topic>Lung Diseases - immunology</topic><topic>Lung Neoplasms</topic><topic>Medical research</topic><topic>Medicine, Experimental</topic><topic>Metabolism</topic><topic>Pediatrics</topic><topic>Peptides</topic><topic>Pharmacology</topic><topic>Phosphorylation</topic><topic>Proteins</topic><topic>Pulmonary arteries</topic><topic>Respiratory tract</topic><topic>Review</topic><topic>Signal Transduction</topic><topic>Signaling</topic><topic>Somatotropin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ma, Lijun</creatorcontrib><creatorcontrib>Wang, Yuming</creatorcontrib><creatorcontrib>Guo, Qiongya</creatorcontrib><creatorcontrib>Li, Wenting</creatorcontrib><creatorcontrib>Wang, Zheng</creatorcontrib><creatorcontrib>Zhang, Xiaoju</creatorcontrib><collection>الدوريات العلمية والإحصائية - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BioMed research international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ma, Lijun</au><au>Wang, Yuming</au><au>Guo, Qiongya</au><au>Li, Wenting</au><au>Wang, Zheng</au><au>Zhang, Xiaoju</au><au>Siafakas, Nikolaos</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Insulin-Like Growth Factor-1 Signaling in Lung Development and Inflammatory Lung Diseases</atitle><jtitle>BioMed research international</jtitle><addtitle>Biomed Res Int</addtitle><date>2018-01-01</date><risdate>2018</risdate><volume>2018</volume><issue>2018</issue><spage>1</spage><epage>27</epage><pages>1-27</pages><issn>2314-6133</issn><eissn>2314-6141</eissn><abstract>Insulin-like growth factor-1 (IGF-1) was firstly identified as a hormone that mediates the biological effects of growth hormone. Accumulating data have indicated the role of IGF-1 signaling pathway in lung development and diseases such as congenital disorders, cancers, inflammation, and fibrosis. IGF-1 signaling modulates the development and differentiation of many types of lung cells, including airway basal cells, club cells, alveolar epithelial cells, and fibroblasts. IGF-1 signaling deficiency results in alveolar hyperplasia in humans and disrupted lung architecture in animal models. The components of IGF-1 signaling pathways are potentiated as biomarkers as they are dysregulated locally or systemically in lung diseases, whereas data may be inconsistent or even paradoxical among different studies. The usage of IGF-1-based therapeutic agents urges for more researches in developmental disorders and inflammatory lung diseases, as the majority of current data are collected from limited number of animal experiments and are generally less exuberant than those in lung cancer. Elucidation of these questions by further bench-to-bedside researches may provide us with rational clinical diagnostic approaches and agents concerning IGF-1 signaling in lung diseases.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>30018981</pmid><doi>10.1155/2018/6057589</doi><tpages>27</tpages><orcidid>https://orcid.org/0000-0002-5189-0993</orcidid><orcidid>https://orcid.org/0000-0001-7734-4838</orcidid><orcidid>https://orcid.org/0000-0002-2833-8746</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Alveoli Animal experimentation Animal models Animal research Animals Apoptosis Basal cells Bioindicators Biological effects Biomarkers Cancer therapies Cell adhesion & migration Cell cycle Chemical compounds Congenital diseases Cystic fibrosis Development and progression Developmental disabilities Diagnostic systems Diseases Disorders Endocrinology Epithelial cells Fibroblasts Fibrosis Growth Hormone Growth hormones Humans Hyperplasia Inflammation Inflammatory diseases Insulin Insulin-like growth factor I Insulin-Like Growth Factor I - physiology Insulin-like growth factors Kinases Ligands Lung - growth & development Lung - pathology Lung cancer Lung diseases Lung Diseases - immunology Lung Neoplasms Medical research Medicine, Experimental Metabolism Pediatrics Peptides Pharmacology Phosphorylation Proteins Pulmonary arteries Respiratory tract Review Signal Transduction Signaling Somatotropin |
title | Insulin-Like Growth Factor-1 Signaling in Lung Development and Inflammatory Lung Diseases |
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