Narrow time window of metabolic changes associated with transition to overt heart failure in Tgaq44 mice
•Glucolytic flux dominates in adaptive hypertrophy and heart failure end-stage.•Increase in fatty acid metabolism characterize transition to overt heart failure.•A causal relationship between structure damage, overactivation PPARα and FA flux in transition phase is suggestive.•Therapeutic time windo...
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| Veröffentlicht in: | Pharmacological reports 2016-08, Vol.68 (4), p.707-714 |
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| creator | Czarnowska, Elżbieta Bierła, Joanna B. Toczek, Marta Tyrankiewicz, Urszula Pająk, Beata Domal-Kwiatkowska, Dorota Ratajska, Anna Smoleński, Ryszard T. Mende, Ulrike Chłopicki, Stefan |
| description | •Glucolytic flux dominates in adaptive hypertrophy and heart failure end-stage.•Increase in fatty acid metabolism characterize transition to overt heart failure.•A causal relationship between structure damage, overactivation PPARα and FA flux in transition phase is suggestive.•Therapeutic time window for modulation of fatty acid metabolism is relatively narrow.
The timing and consequences of alternations in substrate utilization in heart failure (HF) and their relationship with structural changes remain unclear. This study aimed to analyze metabolic changes associated with transition to overt heart failure in transgenic mouse model of HF resulting from cardiac-specific overexpression of constitutively active Gαq*.
Structural changes quantified by morphometry, relative cardiac mRNA and protein expression of PPARα, FAT/CD36, CPT-1, GLUT-4 and glycolytic efficiency following administration of 1-13C glucose were investigated in 4–14-month-old Tgαq*44 mice (TG), compared with age-matched FVB wild type mice (WT).
Initial hypertrophy in TG (4–10-month of age) was featured by an accelerated glycolytic pathway that was not accompanied by structural changes in cardiomyocytes. In 10-month-old TG, cardiomyocyte elongation and hypertrophic remodeling and increased glycolytic flux was accompanied by relatively low expression of FAT/CD36, CPT-1 and PPARα. During the transition phase (12-month-old TG), a pronounced increase in PPARα with an increase in relative fatty acid (FA) flux was associated with anomalies of cardiomyocytes with accumulation of lipid droplets and glycogen as well as cell death. At the stage of overt heart failure (14-month-old TG), an accelerated glycolytic pathway with a decline in FA oxidation was accompanied by further structural changes.
Tgαq*44 mice display three distinct phases of metabolic/structural changes during hypertrophy and progression to HF, with relatively short period of increase in FA metabolism, highlighting a narrow metabolic changes associated with transition to overt heart failure in Tgaq*44 mice that have therapeutic significance. |
| doi_str_mv | 10.1016/j.pharep.2016.03.013 |
| format | Article |
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The timing and consequences of alternations in substrate utilization in heart failure (HF) and their relationship with structural changes remain unclear. This study aimed to analyze metabolic changes associated with transition to overt heart failure in transgenic mouse model of HF resulting from cardiac-specific overexpression of constitutively active Gαq*.
Structural changes quantified by morphometry, relative cardiac mRNA and protein expression of PPARα, FAT/CD36, CPT-1, GLUT-4 and glycolytic efficiency following administration of 1-13C glucose were investigated in 4–14-month-old Tgαq*44 mice (TG), compared with age-matched FVB wild type mice (WT).
Initial hypertrophy in TG (4–10-month of age) was featured by an accelerated glycolytic pathway that was not accompanied by structural changes in cardiomyocytes. In 10-month-old TG, cardiomyocyte elongation and hypertrophic remodeling and increased glycolytic flux was accompanied by relatively low expression of FAT/CD36, CPT-1 and PPARα. During the transition phase (12-month-old TG), a pronounced increase in PPARα with an increase in relative fatty acid (FA) flux was associated with anomalies of cardiomyocytes with accumulation of lipid droplets and glycogen as well as cell death. At the stage of overt heart failure (14-month-old TG), an accelerated glycolytic pathway with a decline in FA oxidation was accompanied by further structural changes.
Tgαq*44 mice display three distinct phases of metabolic/structural changes during hypertrophy and progression to HF, with relatively short period of increase in FA metabolism, highlighting a narrow metabolic changes associated with transition to overt heart failure in Tgaq*44 mice that have therapeutic significance.</description><identifier>ISSN: 1734-1140</identifier><identifier>EISSN: 2299-5684</identifier><identifier>DOI: 10.1016/j.pharep.2016.03.013</identifier><identifier>PMID: 27126697</identifier><language>eng</language><publisher>Cham: Elsevier Urban & Partner Sp. z o.o</publisher><subject>Age Factors ; Animals ; Carnitine O-Palmitoyltransferase - biosynthesis ; CD36 Antigens - biosynthesis ; Cell Death ; Drug Safety and Pharmacovigilance ; Fatty Acids - biosynthesis ; Glucose Transporter Type 4 - biosynthesis ; GTP-Binding Protein alpha Subunits, Gq-G11 - genetics ; Heart failure ; Heart Failure - metabolism ; Heart Failure - pathology ; Hypertrophy ; Hypertrophy - metabolism ; Hypertrophy - pathology ; Metabolic remodeling ; Mice ; Mice, Transgenic ; Myocardium - metabolism ; Myocardium - pathology ; Myocytes, Cardiac - metabolism ; Myocytes, Cardiac - pathology ; Original Research Article ; Pharmacotherapy ; Pharmacy ; PPAR alpha - biosynthesis ; PPARα ; Structural remodeling</subject><ispartof>Pharmacological reports, 2016-08, Vol.68 (4), p.707-714</ispartof><rights>2016 Institute of Pharmacology, Polish Academy of Sciences</rights><rights>Maj Institute of Pharmacology, Polish Academy of Sciences 2016</rights><rights>Copyright © 2016 Institute of Pharmacology, Polish Academy of Sciences. Published by Elsevier Urban & Partner Sp. z o.o. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c338t-17c3b0eda5882b6bc76f48e0c57334bf2342e73c32f0ae13903bcba20f789b8a3</citedby><cites>FETCH-LOGICAL-c338t-17c3b0eda5882b6bc76f48e0c57334bf2342e73c32f0ae13903bcba20f789b8a3</cites><orcidid>0000-0002-8934-9748</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1016/j.pharep.2016.03.013$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1016/j.pharep.2016.03.013$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>315,781,785,27926,27927,41490,42559,51321</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27126697$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Czarnowska, Elżbieta</creatorcontrib><creatorcontrib>Bierła, Joanna B.</creatorcontrib><creatorcontrib>Toczek, Marta</creatorcontrib><creatorcontrib>Tyrankiewicz, Urszula</creatorcontrib><creatorcontrib>Pająk, Beata</creatorcontrib><creatorcontrib>Domal-Kwiatkowska, Dorota</creatorcontrib><creatorcontrib>Ratajska, Anna</creatorcontrib><creatorcontrib>Smoleński, Ryszard T.</creatorcontrib><creatorcontrib>Mende, Ulrike</creatorcontrib><creatorcontrib>Chłopicki, Stefan</creatorcontrib><title>Narrow time window of metabolic changes associated with transition to overt heart failure in Tgaq44 mice</title><title>Pharmacological reports</title><addtitle>Pharmacol. Rep</addtitle><addtitle>Pharmacol Rep</addtitle><description>•Glucolytic flux dominates in adaptive hypertrophy and heart failure end-stage.•Increase in fatty acid metabolism characterize transition to overt heart failure.•A causal relationship between structure damage, overactivation PPARα and FA flux in transition phase is suggestive.•Therapeutic time window for modulation of fatty acid metabolism is relatively narrow.
The timing and consequences of alternations in substrate utilization in heart failure (HF) and their relationship with structural changes remain unclear. This study aimed to analyze metabolic changes associated with transition to overt heart failure in transgenic mouse model of HF resulting from cardiac-specific overexpression of constitutively active Gαq*.
Structural changes quantified by morphometry, relative cardiac mRNA and protein expression of PPARα, FAT/CD36, CPT-1, GLUT-4 and glycolytic efficiency following administration of 1-13C glucose were investigated in 4–14-month-old Tgαq*44 mice (TG), compared with age-matched FVB wild type mice (WT).
Initial hypertrophy in TG (4–10-month of age) was featured by an accelerated glycolytic pathway that was not accompanied by structural changes in cardiomyocytes. In 10-month-old TG, cardiomyocyte elongation and hypertrophic remodeling and increased glycolytic flux was accompanied by relatively low expression of FAT/CD36, CPT-1 and PPARα. During the transition phase (12-month-old TG), a pronounced increase in PPARα with an increase in relative fatty acid (FA) flux was associated with anomalies of cardiomyocytes with accumulation of lipid droplets and glycogen as well as cell death. At the stage of overt heart failure (14-month-old TG), an accelerated glycolytic pathway with a decline in FA oxidation was accompanied by further structural changes.
Tgαq*44 mice display three distinct phases of metabolic/structural changes during hypertrophy and progression to HF, with relatively short period of increase in FA metabolism, highlighting a narrow metabolic changes associated with transition to overt heart failure in Tgaq*44 mice that have therapeutic significance.</description><subject>Age Factors</subject><subject>Animals</subject><subject>Carnitine O-Palmitoyltransferase - biosynthesis</subject><subject>CD36 Antigens - biosynthesis</subject><subject>Cell Death</subject><subject>Drug Safety and Pharmacovigilance</subject><subject>Fatty Acids - biosynthesis</subject><subject>Glucose Transporter Type 4 - biosynthesis</subject><subject>GTP-Binding Protein alpha Subunits, Gq-G11 - genetics</subject><subject>Heart failure</subject><subject>Heart Failure - metabolism</subject><subject>Heart Failure - pathology</subject><subject>Hypertrophy</subject><subject>Hypertrophy - metabolism</subject><subject>Hypertrophy - pathology</subject><subject>Metabolic remodeling</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Myocytes, Cardiac - pathology</subject><subject>Original Research Article</subject><subject>Pharmacotherapy</subject><subject>Pharmacy</subject><subject>PPAR alpha - biosynthesis</subject><subject>PPARα</subject><subject>Structural remodeling</subject><issn>1734-1140</issn><issn>2299-5684</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMtu1TAURS0EoreFP0DIQyYJfiVxJkioKhSpgkkZW8fOSeOrJL61nVb8Pa5SGMLED3ntfeRFyDvOas54-_FYnyaIeKpFudVM1ozLF-QgRN9XTavVS3LgnVQV54qdkfOUjowpLmTzmpyJjou27bsDmb5DjOGRZr8gffTrUM5hpAtmsGH2jroJ1jtMFFIKzkPGoWB5ojnCmnz2YaU50PCAMdMJoawj-HmLSP1Kb-_gXim6eIdvyKsR5oRvn_cL8vPL1e3ldXXz4-u3y883lZNS54p3TlqGAzRaC9ta17Wj0shc00mp7CikEthJJ8XIALnsmbTOgmBjp3urQV6QD3vvKYb7DVM2i08O5xlWDFsyXDOuW654W1C1oy6GlCKO5hT9AvGX4cw8OTZHszs2T44Nk6Y4LrH3zxM2u-DwN_RHagGaHUjlqciL5hi2uJZf_6_4057D4ufBl1xyHleHg4_oshmC_3fBb8O4obo</recordid><startdate>201608</startdate><enddate>201608</enddate><creator>Czarnowska, Elżbieta</creator><creator>Bierła, Joanna B.</creator><creator>Toczek, Marta</creator><creator>Tyrankiewicz, Urszula</creator><creator>Pająk, Beata</creator><creator>Domal-Kwiatkowska, Dorota</creator><creator>Ratajska, Anna</creator><creator>Smoleński, Ryszard T.</creator><creator>Mende, Ulrike</creator><creator>Chłopicki, Stefan</creator><general>Elsevier Urban & Partner Sp. z o.o</general><general>Springer International Publishing</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><orcidid>https://orcid.org/0000-0002-8934-9748</orcidid></search><sort><creationdate>201608</creationdate><title>Narrow time window of metabolic changes associated with transition to overt heart failure in Tgaq44 mice</title><author>Czarnowska, Elżbieta ; Bierła, Joanna B. ; Toczek, Marta ; Tyrankiewicz, Urszula ; Pająk, Beata ; Domal-Kwiatkowska, Dorota ; Ratajska, Anna ; Smoleński, Ryszard T. ; Mende, Ulrike ; Chłopicki, Stefan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c338t-17c3b0eda5882b6bc76f48e0c57334bf2342e73c32f0ae13903bcba20f789b8a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Age Factors</topic><topic>Animals</topic><topic>Carnitine O-Palmitoyltransferase - biosynthesis</topic><topic>CD36 Antigens - biosynthesis</topic><topic>Cell Death</topic><topic>Drug Safety and Pharmacovigilance</topic><topic>Fatty Acids - biosynthesis</topic><topic>Glucose Transporter Type 4 - biosynthesis</topic><topic>GTP-Binding Protein alpha Subunits, Gq-G11 - genetics</topic><topic>Heart failure</topic><topic>Heart Failure - metabolism</topic><topic>Heart Failure - pathology</topic><topic>Hypertrophy</topic><topic>Hypertrophy - metabolism</topic><topic>Hypertrophy - pathology</topic><topic>Metabolic remodeling</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Myocardium - metabolism</topic><topic>Myocardium - pathology</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Myocytes, Cardiac - pathology</topic><topic>Original Research Article</topic><topic>Pharmacotherapy</topic><topic>Pharmacy</topic><topic>PPAR alpha - biosynthesis</topic><topic>PPARα</topic><topic>Structural remodeling</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Czarnowska, Elżbieta</creatorcontrib><creatorcontrib>Bierła, Joanna B.</creatorcontrib><creatorcontrib>Toczek, Marta</creatorcontrib><creatorcontrib>Tyrankiewicz, Urszula</creatorcontrib><creatorcontrib>Pająk, Beata</creatorcontrib><creatorcontrib>Domal-Kwiatkowska, Dorota</creatorcontrib><creatorcontrib>Ratajska, Anna</creatorcontrib><creatorcontrib>Smoleński, Ryszard T.</creatorcontrib><creatorcontrib>Mende, Ulrike</creatorcontrib><creatorcontrib>Chłopicki, Stefan</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><jtitle>Pharmacological reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Czarnowska, Elżbieta</au><au>Bierła, Joanna B.</au><au>Toczek, Marta</au><au>Tyrankiewicz, Urszula</au><au>Pająk, Beata</au><au>Domal-Kwiatkowska, Dorota</au><au>Ratajska, Anna</au><au>Smoleński, Ryszard T.</au><au>Mende, Ulrike</au><au>Chłopicki, Stefan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Narrow time window of metabolic changes associated with transition to overt heart failure in Tgaq44 mice</atitle><jtitle>Pharmacological reports</jtitle><stitle>Pharmacol. Rep</stitle><addtitle>Pharmacol Rep</addtitle><date>2016-08</date><risdate>2016</risdate><volume>68</volume><issue>4</issue><spage>707</spage><epage>714</epage><pages>707-714</pages><issn>1734-1140</issn><eissn>2299-5684</eissn><abstract>•Glucolytic flux dominates in adaptive hypertrophy and heart failure end-stage.•Increase in fatty acid metabolism characterize transition to overt heart failure.•A causal relationship between structure damage, overactivation PPARα and FA flux in transition phase is suggestive.•Therapeutic time window for modulation of fatty acid metabolism is relatively narrow.
The timing and consequences of alternations in substrate utilization in heart failure (HF) and their relationship with structural changes remain unclear. This study aimed to analyze metabolic changes associated with transition to overt heart failure in transgenic mouse model of HF resulting from cardiac-specific overexpression of constitutively active Gαq*.
Structural changes quantified by morphometry, relative cardiac mRNA and protein expression of PPARα, FAT/CD36, CPT-1, GLUT-4 and glycolytic efficiency following administration of 1-13C glucose were investigated in 4–14-month-old Tgαq*44 mice (TG), compared with age-matched FVB wild type mice (WT).
Initial hypertrophy in TG (4–10-month of age) was featured by an accelerated glycolytic pathway that was not accompanied by structural changes in cardiomyocytes. In 10-month-old TG, cardiomyocyte elongation and hypertrophic remodeling and increased glycolytic flux was accompanied by relatively low expression of FAT/CD36, CPT-1 and PPARα. During the transition phase (12-month-old TG), a pronounced increase in PPARα with an increase in relative fatty acid (FA) flux was associated with anomalies of cardiomyocytes with accumulation of lipid droplets and glycogen as well as cell death. At the stage of overt heart failure (14-month-old TG), an accelerated glycolytic pathway with a decline in FA oxidation was accompanied by further structural changes.
Tgαq*44 mice display three distinct phases of metabolic/structural changes during hypertrophy and progression to HF, with relatively short period of increase in FA metabolism, highlighting a narrow metabolic changes associated with transition to overt heart failure in Tgaq*44 mice that have therapeutic significance.</abstract><cop>Cham</cop><pub>Elsevier Urban & Partner Sp. z o.o</pub><pmid>27126697</pmid><doi>10.1016/j.pharep.2016.03.013</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-8934-9748</orcidid></addata></record> |
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| subjects | Age Factors Animals Carnitine O-Palmitoyltransferase - biosynthesis CD36 Antigens - biosynthesis Cell Death Drug Safety and Pharmacovigilance Fatty Acids - biosynthesis Glucose Transporter Type 4 - biosynthesis GTP-Binding Protein alpha Subunits, Gq-G11 - genetics Heart failure Heart Failure - metabolism Heart Failure - pathology Hypertrophy Hypertrophy - metabolism Hypertrophy - pathology Metabolic remodeling Mice Mice, Transgenic Myocardium - metabolism Myocardium - pathology Myocytes, Cardiac - metabolism Myocytes, Cardiac - pathology Original Research Article Pharmacotherapy Pharmacy PPAR alpha - biosynthesis PPARα Structural remodeling |
| title | Narrow time window of metabolic changes associated with transition to overt heart failure in Tgaq44 mice |
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