Fluvastatin inhibits the expression of fibronectin in human peritoneal mesothelial cells induced by high-glucose peritoneal dialysis solution via SGK1 pathway
Background Previous studies showed that statins may have protective effects on peritoneal mesothelial cells (PMC) cultured in high glucose. However, the mechanisms are not clear yet. Several studies demonstrated that serum- and glucocorticoid-inducible kinase 1 (SGK1) is implicated in tissue fibrosi...
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| Veröffentlicht in: | Clinical and experimental nephrology 2015-06, Vol.19 (3), p.336-342 |
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| creator | Zhang, Li Liu, Jia Liu, Yanchun Xu, Yaguang Zhao, Xiufen Qian, Jun Sun, Bin Xing, Changying |
| description | Background
Previous studies showed that statins may have protective effects on peritoneal mesothelial cells (PMC) cultured in high glucose. However, the mechanisms are not clear yet. Several studies demonstrated that serum- and glucocorticoid-inducible kinase 1 (SGK1) is implicated in tissue fibrosis of liver, lung and kidney by regulating the expression of many profibrogenic cytokines and extracellular matrix (e.g., fibronectin). However, few available reports elucidated whether the SGK1 is involved in the pathogenesis of peritoneal fibrosis (PF) in patients with peritoneal dialysis (PD). So far, there is no study about the interaction between the statins and SGK1 in PMC. The purpose of this study was to identify whether fluvastatin may decrease the expression of fibronectin (FN) in human peritoneal mesothelial cells (HPMC) cultured with high-glucose peritoneal dialysis solution (HGPDS) by affecting SGK1 signal pathway.
Methods
Cultured HPMC were divided into groups of control, high-glucose peritoneal dialysis solution (HGPDS), HGPDS with fluvastatin (10
−8
mol/L ~ 10
−6
mol/L) or GSK650394 10
−5
mol/L (the competitive inhibitor of SGK1), fluvastatin 10
−6
mol/L or GSK650394 10
−5
mol/L alone. The expression of SGK1 and FN was detected by RT-PCR, western immunoblotting or ELISA.
Results
Compared with the control, the mRNA and protein expression of SGK1 and FN increased significantly in HPMC treated with HGPDS (
p
|
| doi_str_mv | 10.1007/s10157-014-0991-0 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_1688413704</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3715992631</sourcerecordid><originalsourceid>FETCH-LOGICAL-c521t-4e0bc5ce74a8e4cd3e064b842275cc0b3027d3c424e2a551b000008f3d6727a93</originalsourceid><addsrcrecordid>eNp1kUFv1DAQhS0EoqXwA7ggS5wNY8deJ0dU0YKoxAE4W44z2bjKxsGTtOyf4bfiVQrqhbnMyP7ee4fH2GsJ7ySAfU8SpLECpBbQNFLAE3YudWWFtU3ztNyVVkJaI8_YC6JbAKgb0zxnZ0o3Wu3AnLPfV-N652nxS5x4nIbYxoX4MiDHX3NGopgmnnrexzanCcOG8WE9-InPmONSXv3ID0ipqMZY7oDjSIXq1oAdb498iPtB7Mc1JMLHoq7QR4rEKY3rckq6i55_u_4i-eyX4d4fX7JnvR8JXz3sC_bj6uP3y0_i5uv158sPNyIYJRehEdpgAlrta9ShqxB2uq21UtaEAG0FynZV0Eqj8sbIFk5T91W3s8r6prpgbzffOaefK9LibtOapxLp5K6utaws6ELJjQo5EWXs3Zzjweejk-BOjbitEVcacadGHBTNmwfntT1g90_xt4ICqA2g8jXtMT-K_q_rHzLJmY4</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1688413704</pqid></control><display><type>article</type><title>Fluvastatin inhibits the expression of fibronectin in human peritoneal mesothelial cells induced by high-glucose peritoneal dialysis solution via SGK1 pathway</title><source>MEDLINE</source><source>SpringerNature Journals</source><creator>Zhang, Li ; Liu, Jia ; Liu, Yanchun ; Xu, Yaguang ; Zhao, Xiufen ; Qian, Jun ; Sun, Bin ; Xing, Changying</creator><creatorcontrib>Zhang, Li ; Liu, Jia ; Liu, Yanchun ; Xu, Yaguang ; Zhao, Xiufen ; Qian, Jun ; Sun, Bin ; Xing, Changying</creatorcontrib><description>Background
Previous studies showed that statins may have protective effects on peritoneal mesothelial cells (PMC) cultured in high glucose. However, the mechanisms are not clear yet. Several studies demonstrated that serum- and glucocorticoid-inducible kinase 1 (SGK1) is implicated in tissue fibrosis of liver, lung and kidney by regulating the expression of many profibrogenic cytokines and extracellular matrix (e.g., fibronectin). However, few available reports elucidated whether the SGK1 is involved in the pathogenesis of peritoneal fibrosis (PF) in patients with peritoneal dialysis (PD). So far, there is no study about the interaction between the statins and SGK1 in PMC. The purpose of this study was to identify whether fluvastatin may decrease the expression of fibronectin (FN) in human peritoneal mesothelial cells (HPMC) cultured with high-glucose peritoneal dialysis solution (HGPDS) by affecting SGK1 signal pathway.
Methods
Cultured HPMC were divided into groups of control, high-glucose peritoneal dialysis solution (HGPDS), HGPDS with fluvastatin (10
−8
mol/L ~ 10
−6
mol/L) or GSK650394 10
−5
mol/L (the competitive inhibitor of SGK1), fluvastatin 10
−6
mol/L or GSK650394 10
−5
mol/L alone. The expression of SGK1 and FN was detected by RT-PCR, western immunoblotting or ELISA.
Results
Compared with the control, the mRNA and protein expression of SGK1 and FN increased significantly in HPMC treated with HGPDS (
p
< 0.05). GSK650394 significantly decreased the upregulated mRNA and protein expression of SGK1 and FN induced by HGPDS (
p
< 0.05), and fluvastatin had the same effects as GSK650394 in a dose-dependent manner (
p
< 0.05).
Conclusions
Expression of SGK1 and FN increased in HPMC induced by HGPDS. Treated with fluvastatin and the SGK1-inhibitor GSK650394, abnormalities of SGK1 and FN could be corrected partially, which suggested that the SGK1 pathway was implicated in the pathogenesis of PF, and that fluvastatin might decrease the expression of SGK1 so as to meliorate the progression of PF.</description><identifier>ISSN: 1342-1751</identifier><identifier>EISSN: 1437-7799</identifier><identifier>DOI: 10.1007/s10157-014-0991-0</identifier><identifier>PMID: 24942605</identifier><identifier>CODEN: CENPFV</identifier><language>eng</language><publisher>Tokyo: Springer Japan</publisher><subject>Benzoates - pharmacology ; Bridged Bicyclo Compounds, Heterocyclic - pharmacology ; Cells, Cultured ; Dialysis Solutions - pharmacology ; Epithelial Cells - drug effects ; Epithelial Cells - metabolism ; Fatty Acids, Monounsaturated - antagonists & inhibitors ; Fatty Acids, Monounsaturated - pharmacology ; Fibronectins - genetics ; Fibronectins - metabolism ; Fluvastatin ; Gene Expression - drug effects ; Glucose - pharmacology ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology ; Immediate-Early Proteins - genetics ; Immediate-Early Proteins - metabolism ; Indoles - antagonists & inhibitors ; Indoles - pharmacology ; Medicine ; Medicine & Public Health ; Nephrology ; Original Article ; Peritoneum - cytology ; Protein-Serine-Threonine Kinases - genetics ; Protein-Serine-Threonine Kinases - metabolism ; RNA, Messenger - metabolism ; Signal Transduction - drug effects ; Urology</subject><ispartof>Clinical and experimental nephrology, 2015-06, Vol.19 (3), p.336-342</ispartof><rights>Japanese Society of Nephrology 2014</rights><rights>Japanese Society of Nephrology 2015</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c521t-4e0bc5ce74a8e4cd3e064b842275cc0b3027d3c424e2a551b000008f3d6727a93</citedby><cites>FETCH-LOGICAL-c521t-4e0bc5ce74a8e4cd3e064b842275cc0b3027d3c424e2a551b000008f3d6727a93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10157-014-0991-0$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10157-014-0991-0$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24942605$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Li</creatorcontrib><creatorcontrib>Liu, Jia</creatorcontrib><creatorcontrib>Liu, Yanchun</creatorcontrib><creatorcontrib>Xu, Yaguang</creatorcontrib><creatorcontrib>Zhao, Xiufen</creatorcontrib><creatorcontrib>Qian, Jun</creatorcontrib><creatorcontrib>Sun, Bin</creatorcontrib><creatorcontrib>Xing, Changying</creatorcontrib><title>Fluvastatin inhibits the expression of fibronectin in human peritoneal mesothelial cells induced by high-glucose peritoneal dialysis solution via SGK1 pathway</title><title>Clinical and experimental nephrology</title><addtitle>Clin Exp Nephrol</addtitle><addtitle>Clin Exp Nephrol</addtitle><description>Background
Previous studies showed that statins may have protective effects on peritoneal mesothelial cells (PMC) cultured in high glucose. However, the mechanisms are not clear yet. Several studies demonstrated that serum- and glucocorticoid-inducible kinase 1 (SGK1) is implicated in tissue fibrosis of liver, lung and kidney by regulating the expression of many profibrogenic cytokines and extracellular matrix (e.g., fibronectin). However, few available reports elucidated whether the SGK1 is involved in the pathogenesis of peritoneal fibrosis (PF) in patients with peritoneal dialysis (PD). So far, there is no study about the interaction between the statins and SGK1 in PMC. The purpose of this study was to identify whether fluvastatin may decrease the expression of fibronectin (FN) in human peritoneal mesothelial cells (HPMC) cultured with high-glucose peritoneal dialysis solution (HGPDS) by affecting SGK1 signal pathway.
Methods
Cultured HPMC were divided into groups of control, high-glucose peritoneal dialysis solution (HGPDS), HGPDS with fluvastatin (10
−8
mol/L ~ 10
−6
mol/L) or GSK650394 10
−5
mol/L (the competitive inhibitor of SGK1), fluvastatin 10
−6
mol/L or GSK650394 10
−5
mol/L alone. The expression of SGK1 and FN was detected by RT-PCR, western immunoblotting or ELISA.
Results
Compared with the control, the mRNA and protein expression of SGK1 and FN increased significantly in HPMC treated with HGPDS (
p
< 0.05). GSK650394 significantly decreased the upregulated mRNA and protein expression of SGK1 and FN induced by HGPDS (
p
< 0.05), and fluvastatin had the same effects as GSK650394 in a dose-dependent manner (
p
< 0.05).
Conclusions
Expression of SGK1 and FN increased in HPMC induced by HGPDS. Treated with fluvastatin and the SGK1-inhibitor GSK650394, abnormalities of SGK1 and FN could be corrected partially, which suggested that the SGK1 pathway was implicated in the pathogenesis of PF, and that fluvastatin might decrease the expression of SGK1 so as to meliorate the progression of PF.</description><subject>Benzoates - pharmacology</subject><subject>Bridged Bicyclo Compounds, Heterocyclic - pharmacology</subject><subject>Cells, Cultured</subject><subject>Dialysis Solutions - pharmacology</subject><subject>Epithelial Cells - drug effects</subject><subject>Epithelial Cells - metabolism</subject><subject>Fatty Acids, Monounsaturated - antagonists & inhibitors</subject><subject>Fatty Acids, Monounsaturated - pharmacology</subject><subject>Fibronectins - genetics</subject><subject>Fibronectins - metabolism</subject><subject>Fluvastatin</subject><subject>Gene Expression - drug effects</subject><subject>Glucose - pharmacology</subject><subject>Humans</subject><subject>Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology</subject><subject>Immediate-Early Proteins - genetics</subject><subject>Immediate-Early Proteins - metabolism</subject><subject>Indoles - antagonists & inhibitors</subject><subject>Indoles - pharmacology</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Nephrology</subject><subject>Original Article</subject><subject>Peritoneum - cytology</subject><subject>Protein-Serine-Threonine Kinases - genetics</subject><subject>Protein-Serine-Threonine Kinases - metabolism</subject><subject>RNA, Messenger - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Urology</subject><issn>1342-1751</issn><issn>1437-7799</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kUFv1DAQhS0EoqXwA7ggS5wNY8deJ0dU0YKoxAE4W44z2bjKxsGTtOyf4bfiVQrqhbnMyP7ee4fH2GsJ7ySAfU8SpLECpBbQNFLAE3YudWWFtU3ztNyVVkJaI8_YC6JbAKgb0zxnZ0o3Wu3AnLPfV-N652nxS5x4nIbYxoX4MiDHX3NGopgmnnrexzanCcOG8WE9-InPmONSXv3ID0ipqMZY7oDjSIXq1oAdb498iPtB7Mc1JMLHoq7QR4rEKY3rckq6i55_u_4i-eyX4d4fX7JnvR8JXz3sC_bj6uP3y0_i5uv158sPNyIYJRehEdpgAlrta9ShqxB2uq21UtaEAG0FynZV0Eqj8sbIFk5T91W3s8r6prpgbzffOaefK9LibtOapxLp5K6utaws6ELJjQo5EWXs3Zzjweejk-BOjbitEVcacadGHBTNmwfntT1g90_xt4ICqA2g8jXtMT-K_q_rHzLJmY4</recordid><startdate>20150601</startdate><enddate>20150601</enddate><creator>Zhang, Li</creator><creator>Liu, Jia</creator><creator>Liu, Yanchun</creator><creator>Xu, Yaguang</creator><creator>Zhao, Xiufen</creator><creator>Qian, Jun</creator><creator>Sun, Bin</creator><creator>Xing, Changying</creator><general>Springer Japan</general><general>Springer Nature B.V</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>7QP</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></search><sort><creationdate>20150601</creationdate><title>Fluvastatin inhibits the expression of fibronectin in human peritoneal mesothelial cells induced by high-glucose peritoneal dialysis solution via SGK1 pathway</title><author>Zhang, Li ; Liu, Jia ; Liu, Yanchun ; Xu, Yaguang ; Zhao, Xiufen ; Qian, Jun ; Sun, Bin ; Xing, Changying</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c521t-4e0bc5ce74a8e4cd3e064b842275cc0b3027d3c424e2a551b000008f3d6727a93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Benzoates - pharmacology</topic><topic>Bridged Bicyclo Compounds, Heterocyclic - pharmacology</topic><topic>Cells, Cultured</topic><topic>Dialysis Solutions - pharmacology</topic><topic>Epithelial Cells - drug effects</topic><topic>Epithelial Cells - metabolism</topic><topic>Fatty Acids, Monounsaturated - antagonists & inhibitors</topic><topic>Fatty Acids, Monounsaturated - pharmacology</topic><topic>Fibronectins - genetics</topic><topic>Fibronectins - metabolism</topic><topic>Fluvastatin</topic><topic>Gene Expression - drug effects</topic><topic>Glucose - pharmacology</topic><topic>Humans</topic><topic>Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology</topic><topic>Immediate-Early Proteins - genetics</topic><topic>Immediate-Early Proteins - metabolism</topic><topic>Indoles - antagonists & inhibitors</topic><topic>Indoles - pharmacology</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Nephrology</topic><topic>Original Article</topic><topic>Peritoneum - cytology</topic><topic>Protein-Serine-Threonine Kinases - genetics</topic><topic>Protein-Serine-Threonine Kinases - metabolism</topic><topic>RNA, Messenger - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Urology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Li</creatorcontrib><creatorcontrib>Liu, Jia</creatorcontrib><creatorcontrib>Liu, Yanchun</creatorcontrib><creatorcontrib>Xu, Yaguang</creatorcontrib><creatorcontrib>Zhao, Xiufen</creatorcontrib><creatorcontrib>Qian, Jun</creatorcontrib><creatorcontrib>Sun, Bin</creatorcontrib><creatorcontrib>Xing, Changying</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>Calcium & Calcified Tissue Abstracts</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><jtitle>Clinical and experimental nephrology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Li</au><au>Liu, Jia</au><au>Liu, Yanchun</au><au>Xu, Yaguang</au><au>Zhao, Xiufen</au><au>Qian, Jun</au><au>Sun, Bin</au><au>Xing, Changying</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fluvastatin inhibits the expression of fibronectin in human peritoneal mesothelial cells induced by high-glucose peritoneal dialysis solution via SGK1 pathway</atitle><jtitle>Clinical and experimental nephrology</jtitle><stitle>Clin Exp Nephrol</stitle><addtitle>Clin Exp Nephrol</addtitle><date>2015-06-01</date><risdate>2015</risdate><volume>19</volume><issue>3</issue><spage>336</spage><epage>342</epage><pages>336-342</pages><issn>1342-1751</issn><eissn>1437-7799</eissn><coden>CENPFV</coden><abstract>Background
Previous studies showed that statins may have protective effects on peritoneal mesothelial cells (PMC) cultured in high glucose. However, the mechanisms are not clear yet. Several studies demonstrated that serum- and glucocorticoid-inducible kinase 1 (SGK1) is implicated in tissue fibrosis of liver, lung and kidney by regulating the expression of many profibrogenic cytokines and extracellular matrix (e.g., fibronectin). However, few available reports elucidated whether the SGK1 is involved in the pathogenesis of peritoneal fibrosis (PF) in patients with peritoneal dialysis (PD). So far, there is no study about the interaction between the statins and SGK1 in PMC. The purpose of this study was to identify whether fluvastatin may decrease the expression of fibronectin (FN) in human peritoneal mesothelial cells (HPMC) cultured with high-glucose peritoneal dialysis solution (HGPDS) by affecting SGK1 signal pathway.
Methods
Cultured HPMC were divided into groups of control, high-glucose peritoneal dialysis solution (HGPDS), HGPDS with fluvastatin (10
−8
mol/L ~ 10
−6
mol/L) or GSK650394 10
−5
mol/L (the competitive inhibitor of SGK1), fluvastatin 10
−6
mol/L or GSK650394 10
−5
mol/L alone. The expression of SGK1 and FN was detected by RT-PCR, western immunoblotting or ELISA.
Results
Compared with the control, the mRNA and protein expression of SGK1 and FN increased significantly in HPMC treated with HGPDS (
p
< 0.05). GSK650394 significantly decreased the upregulated mRNA and protein expression of SGK1 and FN induced by HGPDS (
p
< 0.05), and fluvastatin had the same effects as GSK650394 in a dose-dependent manner (
p
< 0.05).
Conclusions
Expression of SGK1 and FN increased in HPMC induced by HGPDS. Treated with fluvastatin and the SGK1-inhibitor GSK650394, abnormalities of SGK1 and FN could be corrected partially, which suggested that the SGK1 pathway was implicated in the pathogenesis of PF, and that fluvastatin might decrease the expression of SGK1 so as to meliorate the progression of PF.</abstract><cop>Tokyo</cop><pub>Springer Japan</pub><pmid>24942605</pmid><doi>10.1007/s10157-014-0991-0</doi><tpages>7</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1342-1751 |
| ispartof | Clinical and experimental nephrology, 2015-06, Vol.19 (3), p.336-342 |
| issn | 1342-1751 1437-7799 |
| language | eng |
| recordid | cdi_proquest_journals_1688413704 |
| source | MEDLINE; SpringerNature Journals |
| subjects | Benzoates - pharmacology Bridged Bicyclo Compounds, Heterocyclic - pharmacology Cells, Cultured Dialysis Solutions - pharmacology Epithelial Cells - drug effects Epithelial Cells - metabolism Fatty Acids, Monounsaturated - antagonists & inhibitors Fatty Acids, Monounsaturated - pharmacology Fibronectins - genetics Fibronectins - metabolism Fluvastatin Gene Expression - drug effects Glucose - pharmacology Humans Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology Immediate-Early Proteins - genetics Immediate-Early Proteins - metabolism Indoles - antagonists & inhibitors Indoles - pharmacology Medicine Medicine & Public Health Nephrology Original Article Peritoneum - cytology Protein-Serine-Threonine Kinases - genetics Protein-Serine-Threonine Kinases - metabolism RNA, Messenger - metabolism Signal Transduction - drug effects Urology |
| title | Fluvastatin inhibits the expression of fibronectin in human peritoneal mesothelial cells induced by high-glucose peritoneal dialysis solution via SGK1 pathway |
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