Renal Mechanisms of Association between Fibroblast Growth Factor 1 and Blood Pressure
The fibroblast growth factor 1 (FGF1) gene is expressed primarily in the kidney and may contribute to hypertension. However, the biologic mechanisms underlying the association between FGF1 and BP regulation remain unknown. We report that the major allele of FGF1 single nucleotide polymorphism rs1525...
Gespeichert in:
Veröffentlicht in: | Journal of the American Society of Nephrology 2015-12, Vol.26 (12), p.3151-3160 |
---|---|
Hauptverfasser: | , , , , , , , , , , , , , , , , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 3160 |
---|---|
container_issue | 12 |
container_start_page | 3151 |
container_title | Journal of the American Society of Nephrology |
container_volume | 26 |
creator | Tomaszewski, Maciej Eales, James Denniff, Matthew Myers, Stephen Chew, Guat Siew Nelson, Christopher P Christofidou, Paraskevi Desai, Aishwarya Büsst, Cara Wojnar, Lukasz Musialik, Katarzyna Jozwiak, Jacek Debiec, Radoslaw Dominiczak, Anna F Navis, Gerjan van Gilst, Wiek H van der Harst, Pim Samani, Nilesh J Harrap, Stephen Bogdanski, Pawel Zukowska-Szczechowska, Ewa Charchar, Fadi J |
description | The fibroblast growth factor 1 (FGF1) gene is expressed primarily in the kidney and may contribute to hypertension. However, the biologic mechanisms underlying the association between FGF1 and BP regulation remain unknown. We report that the major allele of FGF1 single nucleotide polymorphism rs152524 was associated in a dose-dependent manner with systolic BP (P = 9.65 × 10(-5)) and diastolic BP (P = 7.61 × 10(-3)) in a meta-analysis of 14,364 individuals and with renal expression of FGF1 mRNA in 126 human kidneys (P=9.0 × 10(-3)). Next-generation RNA sequencing revealed that upregulated renal expression of FGF1 or of each of the three FGF1 mRNA isoforms individually was associated with higher BP. FGF1-stratified coexpression analysis in two separate collections of human kidneys identified 126 FGF1 partner mRNAs, of which 71 and 63 showed at least nominal association with systolic and diastolic BP, respectively. Of those mRNAs, seven mRNAs in five genes (MME, PTPRO, REN, SLC12A3, and WNK1) had strong prior annotation to BP or hypertension. MME, which encodes an enzyme that degrades circulating natriuretic peptides, showed the strongest differential coexpression with FGF1 between hypertensive and normotensive kidneys. Furthermore, higher level of renal FGF1 expression was associated with lower circulating levels of atrial and brain natriuretic peptides. These findings indicate that FGF1 expression in the kidney is at least under partial genetic control and that renal expression of several FGF1 partner genes involved in the natriuretic peptide catabolism pathway, renin-angiotensin cascade, and sodium handling network may explain the association between FGF1 and BP. |
doi_str_mv | 10.1681/ASN.2014121211 |
format | Article |
fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4657842</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1738815573</sourcerecordid><originalsourceid>FETCH-LOGICAL-c390t-17065ca666994b6d9b6f8e43e1b781721b37654d764857ea1daefee06c5829cd3</originalsourceid><addsrcrecordid>eNpVkUlPxDAMhSMEYr9yRDly6RA3ay9IA2IAiU0s5yhNXaao00DSAfHvKZphkw-25Odnyx8he8BGoAwcju-vRzkDAfkQsEI2QXKecSHZ6lAzoTKlNN8gWyk9MwYy13qdbOSyAMO42iSPd9i5ll6hn7quSbNEQ03HKQXfuL4JHS2xf0fs6KQpYyhbl3p6FsN7P6UT5_sQKVDXVfS4DaGitxFTmkfcIWu1axPuLvM2eZycPpycZ5c3Zxcn48vM84L1GWimpHdKqaIQpaqKUtUGBUcotQGdQ8m1kqLSShip0UHlsEZkykuTF77i2-Ro4fsyL2dYeez66Fr7EpuZix82uMb-73TN1D6FNyuU1Ebkg8HB0iCG1zmm3s6a5LFtXYdhnixobgxIqfkgHS2kPoaUItY_a4DZLxZ2YGF_WQwD-3-P-5F_P59_Aj6MhPE</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1738815573</pqid></control><display><type>article</type><title>Renal Mechanisms of Association between Fibroblast Growth Factor 1 and Blood Pressure</title><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><creator>Tomaszewski, Maciej ; Eales, James ; Denniff, Matthew ; Myers, Stephen ; Chew, Guat Siew ; Nelson, Christopher P ; Christofidou, Paraskevi ; Desai, Aishwarya ; Büsst, Cara ; Wojnar, Lukasz ; Musialik, Katarzyna ; Jozwiak, Jacek ; Debiec, Radoslaw ; Dominiczak, Anna F ; Navis, Gerjan ; van Gilst, Wiek H ; van der Harst, Pim ; Samani, Nilesh J ; Harrap, Stephen ; Bogdanski, Pawel ; Zukowska-Szczechowska, Ewa ; Charchar, Fadi J</creator><creatorcontrib>Tomaszewski, Maciej ; Eales, James ; Denniff, Matthew ; Myers, Stephen ; Chew, Guat Siew ; Nelson, Christopher P ; Christofidou, Paraskevi ; Desai, Aishwarya ; Büsst, Cara ; Wojnar, Lukasz ; Musialik, Katarzyna ; Jozwiak, Jacek ; Debiec, Radoslaw ; Dominiczak, Anna F ; Navis, Gerjan ; van Gilst, Wiek H ; van der Harst, Pim ; Samani, Nilesh J ; Harrap, Stephen ; Bogdanski, Pawel ; Zukowska-Szczechowska, Ewa ; Charchar, Fadi J</creatorcontrib><description>The fibroblast growth factor 1 (FGF1) gene is expressed primarily in the kidney and may contribute to hypertension. However, the biologic mechanisms underlying the association between FGF1 and BP regulation remain unknown. We report that the major allele of FGF1 single nucleotide polymorphism rs152524 was associated in a dose-dependent manner with systolic BP (P = 9.65 × 10(-5)) and diastolic BP (P = 7.61 × 10(-3)) in a meta-analysis of 14,364 individuals and with renal expression of FGF1 mRNA in 126 human kidneys (P=9.0 × 10(-3)). Next-generation RNA sequencing revealed that upregulated renal expression of FGF1 or of each of the three FGF1 mRNA isoforms individually was associated with higher BP. FGF1-stratified coexpression analysis in two separate collections of human kidneys identified 126 FGF1 partner mRNAs, of which 71 and 63 showed at least nominal association with systolic and diastolic BP, respectively. Of those mRNAs, seven mRNAs in five genes (MME, PTPRO, REN, SLC12A3, and WNK1) had strong prior annotation to BP or hypertension. MME, which encodes an enzyme that degrades circulating natriuretic peptides, showed the strongest differential coexpression with FGF1 between hypertensive and normotensive kidneys. Furthermore, higher level of renal FGF1 expression was associated with lower circulating levels of atrial and brain natriuretic peptides. These findings indicate that FGF1 expression in the kidney is at least under partial genetic control and that renal expression of several FGF1 partner genes involved in the natriuretic peptide catabolism pathway, renin-angiotensin cascade, and sodium handling network may explain the association between FGF1 and BP.</description><identifier>ISSN: 1046-6673</identifier><identifier>EISSN: 1533-3450</identifier><identifier>DOI: 10.1681/ASN.2014121211</identifier><identifier>PMID: 25918036</identifier><language>eng</language><publisher>United States: American Society of Nephrology</publisher><subject>Adolescent ; Adult ; Aged ; Blood Pressure - genetics ; Clinical Research ; Female ; Fibroblast Growth Factor 1 - genetics ; Humans ; Hypertension - genetics ; Intracellular Signaling Peptides and Proteins - genetics ; Kidney - chemistry ; Male ; Middle Aged ; Minor Histocompatibility Antigens ; Neprilysin - genetics ; Polymorphism, Single Nucleotide ; Protein Serine-Threonine Kinases - genetics ; Receptor-Like Protein Tyrosine Phosphatases, Class 3 - genetics ; Renin - genetics ; RNA, Messenger - analysis ; Signal Transduction - genetics ; Solute Carrier Family 12, Member 3 - genetics ; WNK Lysine-Deficient Protein Kinase 1 ; Young Adult</subject><ispartof>Journal of the American Society of Nephrology, 2015-12, Vol.26 (12), p.3151-3160</ispartof><rights>Copyright © 2015 by the American Society of Nephrology.</rights><rights>Copyright © 2015 by the American Society of Nephrology 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-17065ca666994b6d9b6f8e43e1b781721b37654d764857ea1daefee06c5829cd3</citedby><cites>FETCH-LOGICAL-c390t-17065ca666994b6d9b6f8e43e1b781721b37654d764857ea1daefee06c5829cd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4657842/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4657842/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25918036$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tomaszewski, Maciej</creatorcontrib><creatorcontrib>Eales, James</creatorcontrib><creatorcontrib>Denniff, Matthew</creatorcontrib><creatorcontrib>Myers, Stephen</creatorcontrib><creatorcontrib>Chew, Guat Siew</creatorcontrib><creatorcontrib>Nelson, Christopher P</creatorcontrib><creatorcontrib>Christofidou, Paraskevi</creatorcontrib><creatorcontrib>Desai, Aishwarya</creatorcontrib><creatorcontrib>Büsst, Cara</creatorcontrib><creatorcontrib>Wojnar, Lukasz</creatorcontrib><creatorcontrib>Musialik, Katarzyna</creatorcontrib><creatorcontrib>Jozwiak, Jacek</creatorcontrib><creatorcontrib>Debiec, Radoslaw</creatorcontrib><creatorcontrib>Dominiczak, Anna F</creatorcontrib><creatorcontrib>Navis, Gerjan</creatorcontrib><creatorcontrib>van Gilst, Wiek H</creatorcontrib><creatorcontrib>van der Harst, Pim</creatorcontrib><creatorcontrib>Samani, Nilesh J</creatorcontrib><creatorcontrib>Harrap, Stephen</creatorcontrib><creatorcontrib>Bogdanski, Pawel</creatorcontrib><creatorcontrib>Zukowska-Szczechowska, Ewa</creatorcontrib><creatorcontrib>Charchar, Fadi J</creatorcontrib><title>Renal Mechanisms of Association between Fibroblast Growth Factor 1 and Blood Pressure</title><title>Journal of the American Society of Nephrology</title><addtitle>J Am Soc Nephrol</addtitle><description>The fibroblast growth factor 1 (FGF1) gene is expressed primarily in the kidney and may contribute to hypertension. However, the biologic mechanisms underlying the association between FGF1 and BP regulation remain unknown. We report that the major allele of FGF1 single nucleotide polymorphism rs152524 was associated in a dose-dependent manner with systolic BP (P = 9.65 × 10(-5)) and diastolic BP (P = 7.61 × 10(-3)) in a meta-analysis of 14,364 individuals and with renal expression of FGF1 mRNA in 126 human kidneys (P=9.0 × 10(-3)). Next-generation RNA sequencing revealed that upregulated renal expression of FGF1 or of each of the three FGF1 mRNA isoforms individually was associated with higher BP. FGF1-stratified coexpression analysis in two separate collections of human kidneys identified 126 FGF1 partner mRNAs, of which 71 and 63 showed at least nominal association with systolic and diastolic BP, respectively. Of those mRNAs, seven mRNAs in five genes (MME, PTPRO, REN, SLC12A3, and WNK1) had strong prior annotation to BP or hypertension. MME, which encodes an enzyme that degrades circulating natriuretic peptides, showed the strongest differential coexpression with FGF1 between hypertensive and normotensive kidneys. Furthermore, higher level of renal FGF1 expression was associated with lower circulating levels of atrial and brain natriuretic peptides. These findings indicate that FGF1 expression in the kidney is at least under partial genetic control and that renal expression of several FGF1 partner genes involved in the natriuretic peptide catabolism pathway, renin-angiotensin cascade, and sodium handling network may explain the association between FGF1 and BP.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Blood Pressure - genetics</subject><subject>Clinical Research</subject><subject>Female</subject><subject>Fibroblast Growth Factor 1 - genetics</subject><subject>Humans</subject><subject>Hypertension - genetics</subject><subject>Intracellular Signaling Peptides and Proteins - genetics</subject><subject>Kidney - chemistry</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Minor Histocompatibility Antigens</subject><subject>Neprilysin - genetics</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Protein Serine-Threonine Kinases - genetics</subject><subject>Receptor-Like Protein Tyrosine Phosphatases, Class 3 - genetics</subject><subject>Renin - genetics</subject><subject>RNA, Messenger - analysis</subject><subject>Signal Transduction - genetics</subject><subject>Solute Carrier Family 12, Member 3 - genetics</subject><subject>WNK Lysine-Deficient Protein Kinase 1</subject><subject>Young Adult</subject><issn>1046-6673</issn><issn>1533-3450</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkUlPxDAMhSMEYr9yRDly6RA3ay9IA2IAiU0s5yhNXaao00DSAfHvKZphkw-25Odnyx8he8BGoAwcju-vRzkDAfkQsEI2QXKecSHZ6lAzoTKlNN8gWyk9MwYy13qdbOSyAMO42iSPd9i5ll6hn7quSbNEQ03HKQXfuL4JHS2xf0fs6KQpYyhbl3p6FsN7P6UT5_sQKVDXVfS4DaGitxFTmkfcIWu1axPuLvM2eZycPpycZ5c3Zxcn48vM84L1GWimpHdKqaIQpaqKUtUGBUcotQGdQ8m1kqLSShip0UHlsEZkykuTF77i2-Ro4fsyL2dYeez66Fr7EpuZix82uMb-73TN1D6FNyuU1Ebkg8HB0iCG1zmm3s6a5LFtXYdhnixobgxIqfkgHS2kPoaUItY_a4DZLxZ2YGF_WQwD-3-P-5F_P59_Aj6MhPE</recordid><startdate>20151201</startdate><enddate>20151201</enddate><creator>Tomaszewski, Maciej</creator><creator>Eales, James</creator><creator>Denniff, Matthew</creator><creator>Myers, Stephen</creator><creator>Chew, Guat Siew</creator><creator>Nelson, Christopher P</creator><creator>Christofidou, Paraskevi</creator><creator>Desai, Aishwarya</creator><creator>Büsst, Cara</creator><creator>Wojnar, Lukasz</creator><creator>Musialik, Katarzyna</creator><creator>Jozwiak, Jacek</creator><creator>Debiec, Radoslaw</creator><creator>Dominiczak, Anna F</creator><creator>Navis, Gerjan</creator><creator>van Gilst, Wiek H</creator><creator>van der Harst, Pim</creator><creator>Samani, Nilesh J</creator><creator>Harrap, Stephen</creator><creator>Bogdanski, Pawel</creator><creator>Zukowska-Szczechowska, Ewa</creator><creator>Charchar, Fadi J</creator><general>American Society of Nephrology</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>20151201</creationdate><title>Renal Mechanisms of Association between Fibroblast Growth Factor 1 and Blood Pressure</title><author>Tomaszewski, Maciej ; Eales, James ; Denniff, Matthew ; Myers, Stephen ; Chew, Guat Siew ; Nelson, Christopher P ; Christofidou, Paraskevi ; Desai, Aishwarya ; Büsst, Cara ; Wojnar, Lukasz ; Musialik, Katarzyna ; Jozwiak, Jacek ; Debiec, Radoslaw ; Dominiczak, Anna F ; Navis, Gerjan ; van Gilst, Wiek H ; van der Harst, Pim ; Samani, Nilesh J ; Harrap, Stephen ; Bogdanski, Pawel ; Zukowska-Szczechowska, Ewa ; Charchar, Fadi J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-17065ca666994b6d9b6f8e43e1b781721b37654d764857ea1daefee06c5829cd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Blood Pressure - genetics</topic><topic>Clinical Research</topic><topic>Female</topic><topic>Fibroblast Growth Factor 1 - genetics</topic><topic>Humans</topic><topic>Hypertension - genetics</topic><topic>Intracellular Signaling Peptides and Proteins - genetics</topic><topic>Kidney - chemistry</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Minor Histocompatibility Antigens</topic><topic>Neprilysin - genetics</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Protein Serine-Threonine Kinases - genetics</topic><topic>Receptor-Like Protein Tyrosine Phosphatases, Class 3 - genetics</topic><topic>Renin - genetics</topic><topic>RNA, Messenger - analysis</topic><topic>Signal Transduction - genetics</topic><topic>Solute Carrier Family 12, Member 3 - genetics</topic><topic>WNK Lysine-Deficient Protein Kinase 1</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tomaszewski, Maciej</creatorcontrib><creatorcontrib>Eales, James</creatorcontrib><creatorcontrib>Denniff, Matthew</creatorcontrib><creatorcontrib>Myers, Stephen</creatorcontrib><creatorcontrib>Chew, Guat Siew</creatorcontrib><creatorcontrib>Nelson, Christopher P</creatorcontrib><creatorcontrib>Christofidou, Paraskevi</creatorcontrib><creatorcontrib>Desai, Aishwarya</creatorcontrib><creatorcontrib>Büsst, Cara</creatorcontrib><creatorcontrib>Wojnar, Lukasz</creatorcontrib><creatorcontrib>Musialik, Katarzyna</creatorcontrib><creatorcontrib>Jozwiak, Jacek</creatorcontrib><creatorcontrib>Debiec, Radoslaw</creatorcontrib><creatorcontrib>Dominiczak, Anna F</creatorcontrib><creatorcontrib>Navis, Gerjan</creatorcontrib><creatorcontrib>van Gilst, Wiek H</creatorcontrib><creatorcontrib>van der Harst, Pim</creatorcontrib><creatorcontrib>Samani, Nilesh J</creatorcontrib><creatorcontrib>Harrap, Stephen</creatorcontrib><creatorcontrib>Bogdanski, Pawel</creatorcontrib><creatorcontrib>Zukowska-Szczechowska, Ewa</creatorcontrib><creatorcontrib>Charchar, Fadi J</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>Journal of the American Society of Nephrology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tomaszewski, Maciej</au><au>Eales, James</au><au>Denniff, Matthew</au><au>Myers, Stephen</au><au>Chew, Guat Siew</au><au>Nelson, Christopher P</au><au>Christofidou, Paraskevi</au><au>Desai, Aishwarya</au><au>Büsst, Cara</au><au>Wojnar, Lukasz</au><au>Musialik, Katarzyna</au><au>Jozwiak, Jacek</au><au>Debiec, Radoslaw</au><au>Dominiczak, Anna F</au><au>Navis, Gerjan</au><au>van Gilst, Wiek H</au><au>van der Harst, Pim</au><au>Samani, Nilesh J</au><au>Harrap, Stephen</au><au>Bogdanski, Pawel</au><au>Zukowska-Szczechowska, Ewa</au><au>Charchar, Fadi J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Renal Mechanisms of Association between Fibroblast Growth Factor 1 and Blood Pressure</atitle><jtitle>Journal of the American Society of Nephrology</jtitle><addtitle>J Am Soc Nephrol</addtitle><date>2015-12-01</date><risdate>2015</risdate><volume>26</volume><issue>12</issue><spage>3151</spage><epage>3160</epage><pages>3151-3160</pages><issn>1046-6673</issn><eissn>1533-3450</eissn><abstract>The fibroblast growth factor 1 (FGF1) gene is expressed primarily in the kidney and may contribute to hypertension. However, the biologic mechanisms underlying the association between FGF1 and BP regulation remain unknown. We report that the major allele of FGF1 single nucleotide polymorphism rs152524 was associated in a dose-dependent manner with systolic BP (P = 9.65 × 10(-5)) and diastolic BP (P = 7.61 × 10(-3)) in a meta-analysis of 14,364 individuals and with renal expression of FGF1 mRNA in 126 human kidneys (P=9.0 × 10(-3)). Next-generation RNA sequencing revealed that upregulated renal expression of FGF1 or of each of the three FGF1 mRNA isoforms individually was associated with higher BP. FGF1-stratified coexpression analysis in two separate collections of human kidneys identified 126 FGF1 partner mRNAs, of which 71 and 63 showed at least nominal association with systolic and diastolic BP, respectively. Of those mRNAs, seven mRNAs in five genes (MME, PTPRO, REN, SLC12A3, and WNK1) had strong prior annotation to BP or hypertension. MME, which encodes an enzyme that degrades circulating natriuretic peptides, showed the strongest differential coexpression with FGF1 between hypertensive and normotensive kidneys. Furthermore, higher level of renal FGF1 expression was associated with lower circulating levels of atrial and brain natriuretic peptides. These findings indicate that FGF1 expression in the kidney is at least under partial genetic control and that renal expression of several FGF1 partner genes involved in the natriuretic peptide catabolism pathway, renin-angiotensin cascade, and sodium handling network may explain the association between FGF1 and BP.</abstract><cop>United States</cop><pub>American Society of Nephrology</pub><pmid>25918036</pmid><doi>10.1681/ASN.2014121211</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1046-6673 |
ispartof | Journal of the American Society of Nephrology, 2015-12, Vol.26 (12), p.3151-3160 |
issn | 1046-6673 1533-3450 |
language | eng |
recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4657842 |
source | MEDLINE; EZB-FREE-00999 freely available EZB journals; PubMed Central |
subjects | Adolescent Adult Aged Blood Pressure - genetics Clinical Research Female Fibroblast Growth Factor 1 - genetics Humans Hypertension - genetics Intracellular Signaling Peptides and Proteins - genetics Kidney - chemistry Male Middle Aged Minor Histocompatibility Antigens Neprilysin - genetics Polymorphism, Single Nucleotide Protein Serine-Threonine Kinases - genetics Receptor-Like Protein Tyrosine Phosphatases, Class 3 - genetics Renin - genetics RNA, Messenger - analysis Signal Transduction - genetics Solute Carrier Family 12, Member 3 - genetics WNK Lysine-Deficient Protein Kinase 1 Young Adult |
title | Renal Mechanisms of Association between Fibroblast Growth Factor 1 and Blood Pressure |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-28T20%3A30%3A25IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Renal%20Mechanisms%20of%20Association%20between%20Fibroblast%20Growth%20Factor%201%20and%20Blood%20Pressure&rft.jtitle=Journal%20of%20the%20American%20Society%20of%20Nephrology&rft.au=Tomaszewski,%20Maciej&rft.date=2015-12-01&rft.volume=26&rft.issue=12&rft.spage=3151&rft.epage=3160&rft.pages=3151-3160&rft.issn=1046-6673&rft.eissn=1533-3450&rft_id=info:doi/10.1681/ASN.2014121211&rft_dat=%3Cproquest_pubme%3E1738815573%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1738815573&rft_id=info:pmid/25918036&rfr_iscdi=true |