Src family kinases in chronic kidney disease
Src family kinases (SFKs) belong to nonreceptor protein tyrosine kinases and have been implicated in the regulation of numerous cellular processes, including cell proliferation, differentiation, migration and invasion, and angiogenesis. The role and mechanisms of SFKs in tumorgenesis have been exten...
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Veröffentlicht in: | American journal of physiology. Renal physiology 2017-09, Vol.313 (3), p.F721-F728 |
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container_title | American journal of physiology. Renal physiology |
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creator | Wang, Jun Zhuang, Shougang |
description | Src family kinases (SFKs) belong to nonreceptor protein tyrosine kinases and have been implicated in the regulation of numerous cellular processes, including cell proliferation, differentiation, migration and invasion, and angiogenesis. The role and mechanisms of SFKs in tumorgenesis have been extensively investigated, and some SFK inhibitors are currently under clinical trials for tumor treatment. Recent studies have also demonstrated the importance of SFKs in regulating the development of various fibrosis-related chronic diseases (e.g., idiopathic pulmonary fibrosis, liver fibrosis, renal fibrosis, and systemic sclerosis). In this article, we summarize the roles of SFKs in various chronic kidney diseases, including glomerulonephritis, diabetic nephropathy, human immunodeficiency virus-associated nephropathy, autosomal dominant form of polycystic kidney disease, and obesity-associated kidney disease, and discuss the mechanisms involved. |
doi_str_mv | 10.1152/ajprenal.00141.2017 |
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The role and mechanisms of SFKs in tumorgenesis have been extensively investigated, and some SFK inhibitors are currently under clinical trials for tumor treatment. Recent studies have also demonstrated the importance of SFKs in regulating the development of various fibrosis-related chronic diseases (e.g., idiopathic pulmonary fibrosis, liver fibrosis, renal fibrosis, and systemic sclerosis). In this article, we summarize the roles of SFKs in various chronic kidney diseases, including glomerulonephritis, diabetic nephropathy, human immunodeficiency virus-associated nephropathy, autosomal dominant form of polycystic kidney disease, and obesity-associated kidney disease, and discuss the mechanisms involved.</description><identifier>ISSN: 1931-857X</identifier><identifier>EISSN: 1522-1466</identifier><identifier>DOI: 10.1152/ajprenal.00141.2017</identifier><identifier>PMID: 28615246</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>Angiogenesis ; Animals ; Cell proliferation ; Clinical trials ; Diabetes mellitus ; Fibrosis ; Glomerulonephritis ; HIV ; Human immunodeficiency virus ; Humans ; Kidney - enzymology ; Kidney - pathology ; Kidney - physiopathology ; Kidney diseases ; Kidney transplantation ; Kinases ; Liver ; Lung diseases ; Nephropathy ; Polycystic kidney ; Prognosis ; Proteins ; Renal Insufficiency, Chronic - enzymology ; Renal Insufficiency, Chronic - pathology ; Renal Insufficiency, Chronic - physiopathology ; Renal Insufficiency, Chronic - therapy ; Review ; Signal Transduction ; Src protein ; src-Family Kinases - metabolism ; Systemic sclerosis ; Tumors ; Tyrosine</subject><ispartof>American journal of physiology. Renal physiology, 2017-09, Vol.313 (3), p.F721-F728</ispartof><rights>Copyright © 2017 the American Physiological Society.</rights><rights>Copyright American Physiological Society Sep 2017</rights><rights>Copyright © 2017 the American Physiological Society 2017 American Physiological Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-d40571e2cdd90d5ef3890201733b0cd38ddcdd88e715f62ca60ea2c82ac4ff473</citedby><cites>FETCH-LOGICAL-c499t-d40571e2cdd90d5ef3890201733b0cd38ddcdd88e715f62ca60ea2c82ac4ff473</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,3025,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28615246$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Jun</creatorcontrib><creatorcontrib>Zhuang, Shougang</creatorcontrib><title>Src family kinases in chronic kidney disease</title><title>American journal of physiology. Renal physiology</title><addtitle>Am J Physiol Renal Physiol</addtitle><description>Src family kinases (SFKs) belong to nonreceptor protein tyrosine kinases and have been implicated in the regulation of numerous cellular processes, including cell proliferation, differentiation, migration and invasion, and angiogenesis. The role and mechanisms of SFKs in tumorgenesis have been extensively investigated, and some SFK inhibitors are currently under clinical trials for tumor treatment. Recent studies have also demonstrated the importance of SFKs in regulating the development of various fibrosis-related chronic diseases (e.g., idiopathic pulmonary fibrosis, liver fibrosis, renal fibrosis, and systemic sclerosis). In this article, we summarize the roles of SFKs in various chronic kidney diseases, including glomerulonephritis, diabetic nephropathy, human immunodeficiency virus-associated nephropathy, autosomal dominant form of polycystic kidney disease, and obesity-associated kidney disease, and discuss the mechanisms involved.</description><subject>Angiogenesis</subject><subject>Animals</subject><subject>Cell proliferation</subject><subject>Clinical trials</subject><subject>Diabetes mellitus</subject><subject>Fibrosis</subject><subject>Glomerulonephritis</subject><subject>HIV</subject><subject>Human immunodeficiency virus</subject><subject>Humans</subject><subject>Kidney - enzymology</subject><subject>Kidney - pathology</subject><subject>Kidney - physiopathology</subject><subject>Kidney diseases</subject><subject>Kidney transplantation</subject><subject>Kinases</subject><subject>Liver</subject><subject>Lung diseases</subject><subject>Nephropathy</subject><subject>Polycystic kidney</subject><subject>Prognosis</subject><subject>Proteins</subject><subject>Renal Insufficiency, Chronic - enzymology</subject><subject>Renal Insufficiency, Chronic - pathology</subject><subject>Renal Insufficiency, Chronic - physiopathology</subject><subject>Renal Insufficiency, Chronic - therapy</subject><subject>Review</subject><subject>Signal Transduction</subject><subject>Src protein</subject><subject>src-Family Kinases - metabolism</subject><subject>Systemic sclerosis</subject><subject>Tumors</subject><subject>Tyrosine</subject><issn>1931-857X</issn><issn>1522-1466</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkUtLAzEUhYMoVqu_QJABNy6cmudMshGk-IKCCxXchTTJ2NRppiYdof_eTF-oq4ScL4dz7wHgDMEBQgxfq-k8WK_qAYSIogGGqNwDR0nBOaJFsZ_ugqCcs_K9B45jnMIEIowOQQ_zInG0OAJXL0FnlZq5epl9Oq-ijZnzmZ6Exjudnoy3y8y4aJN0Ag4qVUd7ujn74O3-7nX4mI-eH56Gt6NcUyEWuaGQlchibYyAhtmKcAG7eISMoTaEG5Mkzm2JWFVgrQpoFdYcK02ripakD27WvvN2PLNGW78Iqpbz4GYqLGWjnPyreDeRH823ZAVmCMFkcLkxCM1Xa-NCzlzUtq6Vt00bJRIJIgVnNKEX_9Bp04a01o5iBHJRii4RWVM6NDEGW-3CICi7NuS2DblqQ67G7YPz33Ps_mzXT34A5A6HsQ</recordid><startdate>20170901</startdate><enddate>20170901</enddate><creator>Wang, Jun</creator><creator>Zhuang, Shougang</creator><general>American Physiological Society</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20170901</creationdate><title>Src family kinases in chronic kidney disease</title><author>Wang, Jun ; Zhuang, Shougang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c499t-d40571e2cdd90d5ef3890201733b0cd38ddcdd88e715f62ca60ea2c82ac4ff473</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Angiogenesis</topic><topic>Animals</topic><topic>Cell proliferation</topic><topic>Clinical trials</topic><topic>Diabetes mellitus</topic><topic>Fibrosis</topic><topic>Glomerulonephritis</topic><topic>HIV</topic><topic>Human immunodeficiency virus</topic><topic>Humans</topic><topic>Kidney - enzymology</topic><topic>Kidney - pathology</topic><topic>Kidney - physiopathology</topic><topic>Kidney diseases</topic><topic>Kidney transplantation</topic><topic>Kinases</topic><topic>Liver</topic><topic>Lung diseases</topic><topic>Nephropathy</topic><topic>Polycystic kidney</topic><topic>Prognosis</topic><topic>Proteins</topic><topic>Renal Insufficiency, Chronic - enzymology</topic><topic>Renal Insufficiency, Chronic - pathology</topic><topic>Renal Insufficiency, Chronic - physiopathology</topic><topic>Renal Insufficiency, Chronic - therapy</topic><topic>Review</topic><topic>Signal Transduction</topic><topic>Src protein</topic><topic>src-Family Kinases - metabolism</topic><topic>Systemic sclerosis</topic><topic>Tumors</topic><topic>Tyrosine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Jun</creatorcontrib><creatorcontrib>Zhuang, Shougang</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>American journal of physiology. Renal physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Jun</au><au>Zhuang, Shougang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Src family kinases in chronic kidney disease</atitle><jtitle>American journal of physiology. Renal physiology</jtitle><addtitle>Am J Physiol Renal Physiol</addtitle><date>2017-09-01</date><risdate>2017</risdate><volume>313</volume><issue>3</issue><spage>F721</spage><epage>F728</epage><pages>F721-F728</pages><issn>1931-857X</issn><eissn>1522-1466</eissn><abstract>Src family kinases (SFKs) belong to nonreceptor protein tyrosine kinases and have been implicated in the regulation of numerous cellular processes, including cell proliferation, differentiation, migration and invasion, and angiogenesis. The role and mechanisms of SFKs in tumorgenesis have been extensively investigated, and some SFK inhibitors are currently under clinical trials for tumor treatment. Recent studies have also demonstrated the importance of SFKs in regulating the development of various fibrosis-related chronic diseases (e.g., idiopathic pulmonary fibrosis, liver fibrosis, renal fibrosis, and systemic sclerosis). In this article, we summarize the roles of SFKs in various chronic kidney diseases, including glomerulonephritis, diabetic nephropathy, human immunodeficiency virus-associated nephropathy, autosomal dominant form of polycystic kidney disease, and obesity-associated kidney disease, and discuss the mechanisms involved.</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>28615246</pmid><doi>10.1152/ajprenal.00141.2017</doi><oa>free_for_read</oa></addata></record> |
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subjects | Angiogenesis Animals Cell proliferation Clinical trials Diabetes mellitus Fibrosis Glomerulonephritis HIV Human immunodeficiency virus Humans Kidney - enzymology Kidney - pathology Kidney - physiopathology Kidney diseases Kidney transplantation Kinases Liver Lung diseases Nephropathy Polycystic kidney Prognosis Proteins Renal Insufficiency, Chronic - enzymology Renal Insufficiency, Chronic - pathology Renal Insufficiency, Chronic - physiopathology Renal Insufficiency, Chronic - therapy Review Signal Transduction Src protein src-Family Kinases - metabolism Systemic sclerosis Tumors Tyrosine |
title | Src family kinases in chronic kidney disease |
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