(Pro)renin Receptor Blockade Ameliorates Heart Failure Caused by Chronic Kidney Disease
The (pro)renin receptor [(P)RR)] is involved in the activation of local renin-angiotensin system and subsequent development of cardiovascular disease. We investigated the therapeutic effect of a (P)RR blocker, handle-region peptide (HRP), on chronic kidney disease (CKD)–associated heart failure. CKD...
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| Veröffentlicht in: | Journal of cardiac failure 2019-04, Vol.25 (4), p.286-300 |
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| creator | Yoshida, Akihiro Kanamori, Hiromitsu Naruse, Genki Minatoguchi, Shingo Iwasa, Masamitsu Yamada, Yoshihisa Mikami, Atsushi Kawasaki, Masanori Nishigaki, Kazuhiko Minatoguchi, Shinya |
| description | The (pro)renin receptor [(P)RR)] is involved in the activation of local renin-angiotensin system and subsequent development of cardiovascular disease. We investigated the therapeutic effect of a (P)RR blocker, handle-region peptide (HRP), on chronic kidney disease (CKD)–associated heart failure.
CKD was induced in C57BL/6J mice by means of five-sixths nephrectomy. Eight weeks later, cardiac dysfunction and cardiac dilatation with hypertension developed. Mice were then assigned to 1 of the 3 following groups: vehicle, low-dose (0.01 mg·kg−1·d−1) HRP, or high-dose (0.3 mg·kg−1·d−1) HRP for 4 weeks. High-dose HRP treatment reversed left ventricular dilation and significantly improved cardiac dysfunction with ameliorated hypertension compared with the vehicle. The hearts with high-dose HRP treatment showed significant attenuation of cardiac fibrosis, cardiomyocyte hypertrophy, macrophage infiltration, and oxidative DNA damage. This treatment decreased the myocardial expressions of angiotensin (Ang) II, Ang II type 1 receptor, transforming growth factor β1, extracellular matrix–related proteins, and lipid peroxidation. Autophagy was activated in the cardiomyocyte from nephrectomized mice, but HRP treatment had no effect on cardiomyocyte autophagy.
This study indicates that (P)PR blockade is a beneficial strategy by suppressing cardiac fibrosis and hypertrophy to ameliorate heart failure caused by CKD. |
| doi_str_mv | 10.1016/j.cardfail.2019.02.009 |
| format | Article |
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CKD was induced in C57BL/6J mice by means of five-sixths nephrectomy. Eight weeks later, cardiac dysfunction and cardiac dilatation with hypertension developed. Mice were then assigned to 1 of the 3 following groups: vehicle, low-dose (0.01 mg·kg−1·d−1) HRP, or high-dose (0.3 mg·kg−1·d−1) HRP for 4 weeks. High-dose HRP treatment reversed left ventricular dilation and significantly improved cardiac dysfunction with ameliorated hypertension compared with the vehicle. The hearts with high-dose HRP treatment showed significant attenuation of cardiac fibrosis, cardiomyocyte hypertrophy, macrophage infiltration, and oxidative DNA damage. This treatment decreased the myocardial expressions of angiotensin (Ang) II, Ang II type 1 receptor, transforming growth factor β1, extracellular matrix–related proteins, and lipid peroxidation. Autophagy was activated in the cardiomyocyte from nephrectomized mice, but HRP treatment had no effect on cardiomyocyte autophagy.
This study indicates that (P)PR blockade is a beneficial strategy by suppressing cardiac fibrosis and hypertrophy to ameliorate heart failure caused by CKD.</description><identifier>ISSN: 1071-9164</identifier><identifier>EISSN: 1532-8414</identifier><identifier>DOI: 10.1016/j.cardfail.2019.02.009</identifier><identifier>PMID: 30769036</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>(Pro)renin receptor ; Animals ; Blotting, Western ; chronic kidney disease ; Disease Models, Animal ; Dose-Response Relationship, Drug ; fibrosis ; Heart Failure - diagnosis ; Heart Failure - etiology ; Heart Failure - prevention & control ; hypertrophy ; Immunohistochemistry ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Microscopy, Electron ; Myocardium - ultrastructure ; Oligopeptides - administration & dosage ; Receptors, Cell Surface - antagonists & inhibitors ; Renal Insufficiency, Chronic - complications ; Renal Insufficiency, Chronic - drug therapy ; Renal Insufficiency, Chronic - metabolism</subject><ispartof>Journal of cardiac failure, 2019-04, Vol.25 (4), p.286-300</ispartof><rights>2019 Elsevier Inc.</rights><rights>Copyright © 2019 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c416t-3828c115d93accdf97f0b14f8f8bf94072660a24f3407ce9db91ec38fa943f4d3</citedby><cites>FETCH-LOGICAL-c416t-3828c115d93accdf97f0b14f8f8bf94072660a24f3407ce9db91ec38fa943f4d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.cardfail.2019.02.009$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,45974</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30769036$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yoshida, Akihiro</creatorcontrib><creatorcontrib>Kanamori, Hiromitsu</creatorcontrib><creatorcontrib>Naruse, Genki</creatorcontrib><creatorcontrib>Minatoguchi, Shingo</creatorcontrib><creatorcontrib>Iwasa, Masamitsu</creatorcontrib><creatorcontrib>Yamada, Yoshihisa</creatorcontrib><creatorcontrib>Mikami, Atsushi</creatorcontrib><creatorcontrib>Kawasaki, Masanori</creatorcontrib><creatorcontrib>Nishigaki, Kazuhiko</creatorcontrib><creatorcontrib>Minatoguchi, Shinya</creatorcontrib><title>(Pro)renin Receptor Blockade Ameliorates Heart Failure Caused by Chronic Kidney Disease</title><title>Journal of cardiac failure</title><addtitle>J Card Fail</addtitle><description>The (pro)renin receptor [(P)RR)] is involved in the activation of local renin-angiotensin system and subsequent development of cardiovascular disease. We investigated the therapeutic effect of a (P)RR blocker, handle-region peptide (HRP), on chronic kidney disease (CKD)–associated heart failure.
CKD was induced in C57BL/6J mice by means of five-sixths nephrectomy. Eight weeks later, cardiac dysfunction and cardiac dilatation with hypertension developed. Mice were then assigned to 1 of the 3 following groups: vehicle, low-dose (0.01 mg·kg−1·d−1) HRP, or high-dose (0.3 mg·kg−1·d−1) HRP for 4 weeks. High-dose HRP treatment reversed left ventricular dilation and significantly improved cardiac dysfunction with ameliorated hypertension compared with the vehicle. The hearts with high-dose HRP treatment showed significant attenuation of cardiac fibrosis, cardiomyocyte hypertrophy, macrophage infiltration, and oxidative DNA damage. This treatment decreased the myocardial expressions of angiotensin (Ang) II, Ang II type 1 receptor, transforming growth factor β1, extracellular matrix–related proteins, and lipid peroxidation. Autophagy was activated in the cardiomyocyte from nephrectomized mice, but HRP treatment had no effect on cardiomyocyte autophagy.
This study indicates that (P)PR blockade is a beneficial strategy by suppressing cardiac fibrosis and hypertrophy to ameliorate heart failure caused by CKD.</description><subject>(Pro)renin receptor</subject><subject>Animals</subject><subject>Blotting, Western</subject><subject>chronic kidney disease</subject><subject>Disease Models, Animal</subject><subject>Dose-Response Relationship, Drug</subject><subject>fibrosis</subject><subject>Heart Failure - diagnosis</subject><subject>Heart Failure - etiology</subject><subject>Heart Failure - prevention & control</subject><subject>hypertrophy</subject><subject>Immunohistochemistry</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>Microscopy, Electron</subject><subject>Myocardium - ultrastructure</subject><subject>Oligopeptides - administration & dosage</subject><subject>Receptors, Cell Surface - antagonists & inhibitors</subject><subject>Renal Insufficiency, Chronic - complications</subject><subject>Renal Insufficiency, Chronic - drug therapy</subject><subject>Renal Insufficiency, Chronic - metabolism</subject><issn>1071-9164</issn><issn>1532-8414</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE9v1DAQxS0EoqXwFSofyyHp-M868Y2ypbRqpVYIxNFy7LHwko0XO0Hab4-rbbn2NO_w3ryZHyGnDFoGTJ1vWmezDzaOLQemW-AtgH5FjtlK8KaXTL6uGjrWaKbkEXlXygYAegndW3IkoFMahDomP88ecvqYcYoT_YYOd3PK9POY3G_rkV5scYwp2xkLvUabZ3pVG5eMdG2Xgp4Oe7r-ldMUHb2NfsI9vYwFbcH35E2wY8EPT_OE_Lj68n193dzdf71ZX9w1TjI1N6LnvWNs5bWwzvmguwADk6EP_RB0PZYrBZbLIKp2qP2gGTrRB6ulCNKLE3J22LvL6c-CZTbbWByOo50wLcVwpgVTXHWralUHq8uplIzB7HLc2rw3DMwjVLMxz1DNI1QD3FSoNXj61LEMW_T_Y88Uq-HTwYD1078Rsyku4uTQx4xuNj7Flzr-AdyvizE</recordid><startdate>201904</startdate><enddate>201904</enddate><creator>Yoshida, Akihiro</creator><creator>Kanamori, Hiromitsu</creator><creator>Naruse, Genki</creator><creator>Minatoguchi, Shingo</creator><creator>Iwasa, Masamitsu</creator><creator>Yamada, Yoshihisa</creator><creator>Mikami, Atsushi</creator><creator>Kawasaki, Masanori</creator><creator>Nishigaki, Kazuhiko</creator><creator>Minatoguchi, Shinya</creator><general>Elsevier Inc</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></search><sort><creationdate>201904</creationdate><title>(Pro)renin Receptor Blockade Ameliorates Heart Failure Caused by Chronic Kidney Disease</title><author>Yoshida, Akihiro ; Kanamori, Hiromitsu ; Naruse, Genki ; Minatoguchi, Shingo ; Iwasa, Masamitsu ; Yamada, Yoshihisa ; Mikami, Atsushi ; Kawasaki, Masanori ; Nishigaki, Kazuhiko ; Minatoguchi, Shinya</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c416t-3828c115d93accdf97f0b14f8f8bf94072660a24f3407ce9db91ec38fa943f4d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>(Pro)renin receptor</topic><topic>Animals</topic><topic>Blotting, Western</topic><topic>chronic kidney disease</topic><topic>Disease Models, Animal</topic><topic>Dose-Response Relationship, Drug</topic><topic>fibrosis</topic><topic>Heart Failure - diagnosis</topic><topic>Heart Failure - etiology</topic><topic>Heart Failure - prevention & control</topic><topic>hypertrophy</topic><topic>Immunohistochemistry</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Transgenic</topic><topic>Microscopy, Electron</topic><topic>Myocardium - ultrastructure</topic><topic>Oligopeptides - administration & dosage</topic><topic>Receptors, Cell Surface - antagonists & inhibitors</topic><topic>Renal Insufficiency, Chronic - complications</topic><topic>Renal Insufficiency, Chronic - drug therapy</topic><topic>Renal Insufficiency, Chronic - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yoshida, Akihiro</creatorcontrib><creatorcontrib>Kanamori, Hiromitsu</creatorcontrib><creatorcontrib>Naruse, Genki</creatorcontrib><creatorcontrib>Minatoguchi, Shingo</creatorcontrib><creatorcontrib>Iwasa, Masamitsu</creatorcontrib><creatorcontrib>Yamada, Yoshihisa</creatorcontrib><creatorcontrib>Mikami, Atsushi</creatorcontrib><creatorcontrib>Kawasaki, Masanori</creatorcontrib><creatorcontrib>Nishigaki, Kazuhiko</creatorcontrib><creatorcontrib>Minatoguchi, Shinya</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>Journal of cardiac failure</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yoshida, Akihiro</au><au>Kanamori, Hiromitsu</au><au>Naruse, Genki</au><au>Minatoguchi, Shingo</au><au>Iwasa, Masamitsu</au><au>Yamada, Yoshihisa</au><au>Mikami, Atsushi</au><au>Kawasaki, Masanori</au><au>Nishigaki, Kazuhiko</au><au>Minatoguchi, Shinya</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>(Pro)renin Receptor Blockade Ameliorates Heart Failure Caused by Chronic Kidney Disease</atitle><jtitle>Journal of cardiac failure</jtitle><addtitle>J Card Fail</addtitle><date>2019-04</date><risdate>2019</risdate><volume>25</volume><issue>4</issue><spage>286</spage><epage>300</epage><pages>286-300</pages><issn>1071-9164</issn><eissn>1532-8414</eissn><abstract>The (pro)renin receptor [(P)RR)] is involved in the activation of local renin-angiotensin system and subsequent development of cardiovascular disease. We investigated the therapeutic effect of a (P)RR blocker, handle-region peptide (HRP), on chronic kidney disease (CKD)–associated heart failure.
CKD was induced in C57BL/6J mice by means of five-sixths nephrectomy. Eight weeks later, cardiac dysfunction and cardiac dilatation with hypertension developed. Mice were then assigned to 1 of the 3 following groups: vehicle, low-dose (0.01 mg·kg−1·d−1) HRP, or high-dose (0.3 mg·kg−1·d−1) HRP for 4 weeks. High-dose HRP treatment reversed left ventricular dilation and significantly improved cardiac dysfunction with ameliorated hypertension compared with the vehicle. The hearts with high-dose HRP treatment showed significant attenuation of cardiac fibrosis, cardiomyocyte hypertrophy, macrophage infiltration, and oxidative DNA damage. This treatment decreased the myocardial expressions of angiotensin (Ang) II, Ang II type 1 receptor, transforming growth factor β1, extracellular matrix–related proteins, and lipid peroxidation. Autophagy was activated in the cardiomyocyte from nephrectomized mice, but HRP treatment had no effect on cardiomyocyte autophagy.
This study indicates that (P)PR blockade is a beneficial strategy by suppressing cardiac fibrosis and hypertrophy to ameliorate heart failure caused by CKD.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>30769036</pmid><doi>10.1016/j.cardfail.2019.02.009</doi><tpages>15</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Journal of cardiac failure, 2019-04, Vol.25 (4), p.286-300 |
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| subjects | (Pro)renin receptor Animals Blotting, Western chronic kidney disease Disease Models, Animal Dose-Response Relationship, Drug fibrosis Heart Failure - diagnosis Heart Failure - etiology Heart Failure - prevention & control hypertrophy Immunohistochemistry Male Mice Mice, Inbred C57BL Mice, Transgenic Microscopy, Electron Myocardium - ultrastructure Oligopeptides - administration & dosage Receptors, Cell Surface - antagonists & inhibitors Renal Insufficiency, Chronic - complications Renal Insufficiency, Chronic - drug therapy Renal Insufficiency, Chronic - metabolism |
| title | (Pro)renin Receptor Blockade Ameliorates Heart Failure Caused by Chronic Kidney Disease |
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