The impact of galectin-3 inhibition on aldosterone-induced cardiac and renal injuries.
Identifieur interne : 000062 ( PubMed/Corpus ); précédent : 000061; suivant : 000063The impact of galectin-3 inhibition on aldosterone-induced cardiac and renal injuries.
Auteurs : Laurent Calvier ; Ernesto Martinez-Martinez ; Maria Miana ; Victoria Cachofeiro ; Elodie Rousseau ; J Rafael Sádaba ; Faiez Zannad ; Patrick Rossignol ; Natalia L Pez-AndrésSource :
- JACC. Heart failure [ 2213-1787 ] ; 2015.
English descriptors
- KwdEn :
- Acute Kidney Injury (chemically induced), Acute Kidney Injury (drug therapy), Acute Kidney Injury (metabolism), Aldosterone (toxicity), Animals, Disease Models, Animal, Enzyme-Linked Immunosorbent Assay, Galectin 3 (antagonists & inhibitors), Galectin 3 (biosynthesis), Heart Failure (chemically induced), Heart Failure (drug therapy), Heart Failure (metabolism), Immunohistochemistry, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Mineralocorticoid Receptor Antagonists (therapeutic use), Rats, Rats, Wistar, Spironolactone (therapeutic use).
- MESH :
- chemical , antagonists & inhibitors : Galectin 3.
- chemical , biosynthesis : Galectin 3.
- chemical , therapeutic use : Mineralocorticoid Receptor Antagonists, Spironolactone.
- chemical , toxicity : Aldosterone.
- chemically induced : Acute Kidney Injury, Heart Failure.
- drug therapy : Acute Kidney Injury, Heart Failure.
- metabolism : Acute Kidney Injury, Heart Failure.
- Animals, Disease Models, Animal, Enzyme-Linked Immunosorbent Assay, Immunohistochemistry, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Rats, Rats, Wistar.
Abstract
This study investigated whether galectin (Gal)-3 inhibition could block aldosterone-induced cardiac and renal fibrosis and improve cardiorenal dysfunction.
DOI: 10.1016/j.jchf.2014.08.002
PubMed: 25458174
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pubmed:25458174Le document en format XML
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Electronic address: natalia.lopez.andres@navarra.es.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2015">2015</date><idno type="RBID">pubmed:25458174</idno><idno type="pmid">25458174</idno><idno type="doi">10.1016/j.jchf.2014.08.002</idno><idno type="wicri:Area/PubMed/Corpus">000062</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000062</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">The impact of galectin-3 inhibition on aldosterone-induced cardiac and renal injuries.</title><author><name sortKey="Calvier, Laurent" sort="Calvier, Laurent" uniqKey="Calvier L" first="Laurent" last="Calvier">Laurent Calvier</name><affiliation><nlm:affiliation>INSERM, Université de Lorraine UMR 1116, Vandoeuvre-Lès-Nancy, France.</nlm:affiliation></affiliation></author><author><name sortKey="Martinez Martinez, Ernesto" sort="Martinez Martinez, Ernesto" uniqKey="Martinez Martinez E" first="Ernesto" last="Martinez-Martinez">Ernesto Martinez-Martinez</name><affiliation><nlm:affiliation>Universidad Complutense de Madrid, Madrid, Spain; Navarrabiomed-Fundación Miguel Servet, Pamplona, Spain.</nlm:affiliation></affiliation></author><author><name sortKey="Miana, Maria" sort="Miana, Maria" uniqKey="Miana M" first="Maria" last="Miana">Maria Miana</name><affiliation><nlm:affiliation>Universidad Complutense de Madrid, Madrid, Spain.</nlm:affiliation></affiliation></author><author><name sortKey="Cachofeiro, Victoria" sort="Cachofeiro, Victoria" uniqKey="Cachofeiro V" first="Victoria" last="Cachofeiro">Victoria Cachofeiro</name><affiliation><nlm:affiliation>Universidad Complutense de Madrid, Madrid, Spain.</nlm:affiliation></affiliation></author><author><name sortKey="Rousseau, Elodie" sort="Rousseau, Elodie" uniqKey="Rousseau E" first="Elodie" last="Rousseau">Elodie Rousseau</name><affiliation><nlm:affiliation>INSERM, Université de Lorraine UMR 1116, Vandoeuvre-Lès-Nancy, France.</nlm:affiliation></affiliation></author><author><name sortKey="Sadaba, J Rafael" sort="Sadaba, J Rafael" uniqKey="Sadaba J" first="J Rafael" last="Sádaba">J Rafael Sádaba</name><affiliation><nlm:affiliation>Navarrabiomed-Fundación Miguel Servet, Pamplona, Spain; Department of Cardiac Surgery, Complejo Hospitalario de Navarra, Pamplona, Spain.</nlm:affiliation></affiliation></author><author><name sortKey="Zannad, Faiez" sort="Zannad, Faiez" uniqKey="Zannad F" first="Faiez" last="Zannad">Faiez Zannad</name><affiliation><nlm:affiliation>INSERM, Université de Lorraine UMR 1116, Vandoeuvre-Lès-Nancy, France; CHU Nancy, INSERM Clinical Investigation Center, CIC 9501, Vandoeuvre-Lès-Nancy, France; F-CRIN INI-CRCT (Cardiovascular and Renal Clinical Trialists), Nancy, France.</nlm:affiliation></affiliation></author><author><name sortKey="Rossignol, Patrick" sort="Rossignol, Patrick" uniqKey="Rossignol P" first="Patrick" last="Rossignol">Patrick Rossignol</name><affiliation><nlm:affiliation>INSERM, Université de Lorraine UMR 1116, Vandoeuvre-Lès-Nancy, France; CHU Nancy, INSERM Clinical Investigation Center, CIC 9501, Vandoeuvre-Lès-Nancy, France; F-CRIN INI-CRCT (Cardiovascular and Renal Clinical Trialists), Nancy, France.</nlm:affiliation></affiliation></author><author><name sortKey="L Pez Andres, Natalia" sort="L Pez Andres, Natalia" uniqKey="L Pez Andres N" first="Natalia" last="L Pez-Andrés">Natalia L Pez-Andrés</name><affiliation><nlm:affiliation>INSERM, Université de Lorraine UMR 1116, Vandoeuvre-Lès-Nancy, France; Navarrabiomed-Fundación Miguel Servet, Pamplona, Spain. Electronic address: natalia.lopez.andres@navarra.es.</nlm:affiliation></affiliation></author></analytic><series><title level="j">JACC. Heart failure</title><idno type="eISSN">2213-1787</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acute Kidney Injury (chemically induced)</term><term>Acute Kidney Injury (drug therapy)</term><term>Acute Kidney Injury (metabolism)</term><term>Aldosterone (toxicity)</term><term>Animals</term><term>Disease Models, Animal</term><term>Enzyme-Linked Immunosorbent Assay</term><term>Galectin 3 (antagonists & inhibitors)</term><term>Galectin 3 (biosynthesis)</term><term>Heart Failure (chemically induced)</term><term>Heart Failure (drug therapy)</term><term>Heart Failure (metabolism)</term><term>Immunohistochemistry</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term><term>Mineralocorticoid Receptor Antagonists (therapeutic use)</term><term>Rats</term><term>Rats, Wistar</term><term>Spironolactone (therapeutic use)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Galectin 3</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Galectin 3</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Mineralocorticoid Receptor Antagonists</term><term>Spironolactone</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Aldosterone</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Acute Kidney Injury</term><term>Heart Failure</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Acute Kidney Injury</term><term>Heart Failure</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Acute Kidney Injury</term><term>Heart Failure</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Enzyme-Linked Immunosorbent Assay</term><term>Immunohistochemistry</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term><term>Rats</term><term>Rats, Wistar</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">This study investigated whether galectin (Gal)-3 inhibition could block aldosterone-induced cardiac and renal fibrosis and improve cardiorenal dysfunction.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">25458174</PMID><DateCreated><Year>2015</Year><Month>01</Month><Day>09</Day></DateCreated><DateCompleted><Year>2015</Year><Month>10</Month><Day>06</Day></DateCompleted><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">2213-1787</ISSN><JournalIssue CitedMedium="Internet"><Volume>3</Volume><Issue>1</Issue><PubDate><Year>2015</Year><Month>Jan</Month></PubDate></JournalIssue><Title>JACC. Heart failure</Title><ISOAbbreviation>JACC Heart Fail</ISOAbbreviation></Journal><ArticleTitle>The impact of galectin-3 inhibition on aldosterone-induced cardiac and renal injuries.</ArticleTitle><Pagination><MedlinePgn>59-67</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.jchf.2014.08.002</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S2213-1779(14)00388-6</ELocationID><Abstract><AbstractText Label="OBJECTIVES" NlmCategory="OBJECTIVE">This study investigated whether galectin (Gal)-3 inhibition could block aldosterone-induced cardiac and renal fibrosis and improve cardiorenal dysfunction.</AbstractText><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Aldosterone is involved in cardiac and renal fibrosis that is associated with the development of cardiorenal injury. However, the mechanisms of these interactions remain unclear. Gal-3, a β-galactoside-binding lectin, is increased in heart failure and kidney injury.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">Rats were treated with aldosterone-salt combined with spironolactone (a mineralocorticoid receptor antagonist) or modified citrus pectin (a Gal-3 inhibitor), for 3 weeks. Wild-type and Gal-3 knockout mice were treated with aldosterone for 3 weeks. Hemodynamic, cardiac, and renal parameters were analyzed.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Hypertensive aldosterone-salt-treated rats presented cardiac and renal hypertrophy (at morphometric, cellular, and molecular levels) and dysfunction. Cardiac and renal expressions of Gal-3 as well as levels of molecular markers attesting fibrosis were also augmented by aldosterone-salt treatment. Spironolactone or modified citrus pectin treatment reversed all of these effects. In wild-type mice, aldosterone did not alter blood pressure levels but increased cardiac and renal Gal-3 expression, fibrosis, and renal epithelial-mesenchymal transition. Gal-3 knockout mice were resistant to aldosterone effects.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">In experimental hyperaldosteronism, the increase in Gal-3 expression was associated with cardiac and renal fibrosis and dysfunction but was prevented by pharmacological inhibition (modified citrus pectin) or genetic disruption of Gal-3. These data suggest a key role for Gal-3 in cardiorenal remodeling and dysfunction induced by aldosterone. Gal-3 could be used as a new biotarget for specific pharmacological interventions.</AbstractText><CopyrightInformation>Copyright © 2015 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Calvier</LastName><ForeName>Laurent</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>INSERM, Université de Lorraine UMR 1116, Vandoeuvre-Lès-Nancy, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Martinez-Martinez</LastName><ForeName>Ernesto</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Universidad Complutense de Madrid, Madrid, Spain; Navarrabiomed-Fundación Miguel Servet, Pamplona, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Miana</LastName><ForeName>Maria</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Universidad Complutense de Madrid, Madrid, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cachofeiro</LastName><ForeName>Victoria</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Universidad Complutense de Madrid, Madrid, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rousseau</LastName><ForeName>Elodie</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>INSERM, Université de Lorraine UMR 1116, Vandoeuvre-Lès-Nancy, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sádaba</LastName><ForeName>J Rafael</ForeName><Initials>JR</Initials><AffiliationInfo><Affiliation>Navarrabiomed-Fundación Miguel Servet, Pamplona, Spain; Department of Cardiac Surgery, Complejo Hospitalario de Navarra, Pamplona, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zannad</LastName><ForeName>Faiez</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>INSERM, Université de Lorraine UMR 1116, Vandoeuvre-Lès-Nancy, France; CHU Nancy, INSERM Clinical Investigation Center, CIC 9501, Vandoeuvre-Lès-Nancy, France; F-CRIN INI-CRCT (Cardiovascular and Renal Clinical Trialists), Nancy, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rossignol</LastName><ForeName>Patrick</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>INSERM, Université de Lorraine UMR 1116, Vandoeuvre-Lès-Nancy, France; CHU Nancy, INSERM Clinical Investigation Center, CIC 9501, Vandoeuvre-Lès-Nancy, France; F-CRIN INI-CRCT (Cardiovascular and Renal Clinical Trialists), Nancy, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>López-Andrés</LastName><ForeName>Natalia</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>INSERM, Université de Lorraine UMR 1116, Vandoeuvre-Lès-Nancy, France; Navarrabiomed-Fundación Miguel Servet, Pamplona, Spain. Electronic address: natalia.lopez.andres@navarra.es.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>11</Month><Day>11</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>JACC Heart Fail</MedlineTA><NlmUniqueID>101598241</NlmUniqueID><ISSNLinking>2213-1779</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D037502">Galectin 3</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000451">Mineralocorticoid Receptor Antagonists</NameOfSubstance></Chemical><Chemical><RegistryNumber>27O7W4T232</RegistryNumber><NameOfSubstance UI="D013148">Spironolactone</NameOfSubstance></Chemical><Chemical><RegistryNumber>4964P6T9RB</RegistryNumber><NameOfSubstance UI="D000450">Aldosterone</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>JACC Heart Fail. 2015 Jan;3(1):68-9</RefSource><PMID Version="1">25458173</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D058186">Acute Kidney Injury</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000139">chemically induced</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000188">drug therapy</QualifierName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000450">Aldosterone</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000633">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000818">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004195">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004797">Enzyme-Linked Immunosorbent Assay</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D037502">Galectin 3</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000037">antagonists & inhibitors</QualifierName><QualifierName MajorTopicYN="N" UI="Q000096">biosynthesis</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006333">Heart Failure</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000139">chemically induced</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000188">drug therapy</QualifierName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007150">Immunohistochemistry</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D051379">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008810">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D018345">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000451">Mineralocorticoid Receptor Antagonists</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D051381">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D017208">Rats, Wistar</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D013148">Spironolactone</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000627">therapeutic use</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">aldosterone</Keyword><Keyword MajorTopicYN="N">biomarker</Keyword><Keyword MajorTopicYN="N">cardiorenal injury</Keyword><Keyword MajorTopicYN="N">collagen</Keyword><Keyword MajorTopicYN="N">galectin-3</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2014</Year><Month>6</Month><Day>9</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2014</Year><Month>8</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2014</Year><Month>8</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="aheadofprint"><Year>2014</Year><Month>11</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>12</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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