{"created":"2021-03-01T06:30:50.155837+00:00","id":23018,"links":{},"metadata":{"_buckets":{"deposit":"406ddefa-7a11-45e9-9c65-2d0eca745a42"},"_deposit":{"id":"23018","owners":[],"pid":{"revision_id":0,"type":"depid","value":"23018"},"status":"published"},"_oai":{"id":"oai:nagoya.repo.nii.ac.jp:00023018","sets":["499:500:501"]},"author_link":["68032","68033","68034","68035","68036","68037"],"item_10_biblio_info_6":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2016-09","bibliographicIssueDateType":"Issued"},"bibliographicPageEnd":"47","bibliographicPageStart":"37","bibliographicVolumeNumber":"98","bibliographic_titles":[{"bibliographic_title":"Journal of Molecular and Cellular Cardiology","bibliographic_titleLang":"en"}]}]},"item_10_description_4":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"Background: To address the impact of antidiabetic drugs on cardiovascular safety is a matter of clinical concern. Preclinical studies revealed that various protective effects of dipeptidyl peptidase-4 inhibitor (DPP4i) on cardiovascular disease; however, its impact of on hypertension remains controversial. Methods and results: Teneligliptin (TEN; 10 mg/kg/day/p.o.) ameliorates hypertension and cardiac remodeling by normalizing a rise of angiotensin-II (AngII) that specifically observed in spontaneously hypertensive rats (SHR). TEN had no effects on vasculature and concentrations of the DPP4-related vasoactive peptides (bradykinin, neuropeptide Y, and atrial natriuretic peptide). The primary action of TEN on BP lowering was due to restoring the AngII-induced manifestation of congestive heart failure observed in SHR. Sodium-proton pump exchanger type 1 (NHE-1) is a regulator of intracellular acidity (pHi) and implicated pathophysiological role in cardiac remodeling occurred in diseased myocardium. Cardiac NHE-1 expression level was increased in SHR and this was restored in TEN-treated SHR. AngII directly augmented cardiac NHE-1 expression and its activity that contributed to hypertrophic response. TEN attenuated the AngII-induced cardiac hypertrophy with decline in pHi via suppression of NHE-1. Loss of NHE-1 activity by specific inhibitor or RNA silencing promoted intracellular acidification and consistently attenuated the AngII-mediated cardiac hypertrophy. Conclusion: The present study revealed the protective actions of TEN on hypertension and comorbid cardiac remodeling via AngII/NHE-1 axis and the novel pathophysiological roles of intracellular acidification via NHE-1 in cardiac hypertrophy.","subitem_description_language":"en","subitem_description_type":"Abstract"}]},"item_10_identifier_60":{"attribute_name":"URI","attribute_value_mlt":[{"subitem_identifier_type":"DOI","subitem_identifier_uri":"http://doi.org/10.1016/j.yjmcc.2016.06.066"},{"subitem_identifier_type":"HDL","subitem_identifier_uri":"http://hdl.handle.net/2237/25205"}]},"item_10_publisher_32":{"attribute_name":"出版者","attribute_value_mlt":[{"subitem_publisher":"Elsevier","subitem_publisher_language":"en"}]},"item_10_relation_11":{"attribute_name":"DOI","attribute_value_mlt":[{"subitem_relation_type":"isVersionOf","subitem_relation_type_id":{"subitem_relation_type_id_text":"https://doi.org/10.1016/j.yjmcc.2016.06.066","subitem_relation_type_select":"DOI"}}]},"item_10_rights_12":{"attribute_name":"権利","attribute_value_mlt":[{"subitem_rights":"© 2016. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/","subitem_rights_language":"en"}]},"item_10_select_15":{"attribute_name":"著者版フラグ","attribute_value_mlt":[{"subitem_select_item":"author"}]},"item_10_source_id_7":{"attribute_name":"ISSN","attribute_value_mlt":[{"subitem_source_identifier":"0022-2828","subitem_source_identifier_type":"PISSN"}]},"item_1615787544753":{"attribute_name":"出版タイプ","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_ab4af688f83e57aa","subitem_version_type":"AM"}]},"item_access_right":{"attribute_name":"アクセス権","attribute_value_mlt":[{"subitem_access_right":"open access","subitem_access_right_uri":"http://purl.org/coar/access_right/c_abf2"}]},"item_creator":{"attribute_name":"著者","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"Kawase, Haruya","creatorNameLang":"en"}],"nameIdentifiers":[{"nameIdentifier":"68032","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"Bando, K.  Yasuko","creatorNameLang":"en"}],"nameIdentifiers":[{"nameIdentifier":"68033","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"Nishimura, Kazuyuki","creatorNameLang":"en"}],"nameIdentifiers":[{"nameIdentifier":"68034","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"Aoyama, Morihiko","creatorNameLang":"en"}],"nameIdentifiers":[{"nameIdentifier":"68035","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"Monji, Akio","creatorNameLang":"en"}],"nameIdentifiers":[{"nameIdentifier":"68036","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"Murohara, Toyoaki","creatorNameLang":"en"}],"nameIdentifiers":[{"nameIdentifier":"68037","nameIdentifierScheme":"WEKO"}]}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2017-09-01"}],"displaytype":"detail","filename":"Final-20160626-HK-Manuscript-Main.pdf","filesize":[{"value":"317.2 kB"}],"format":"application/pdf","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"Final-20160626-HK-Manuscript-Main.pdf ファイル公開：2017/09/01","objectType":"fulltext","url":"https://nagoya.repo.nii.ac.jp/record/23018/files/Final-20160626-HK-Manuscript-Main.pdf"},"version_id":"d5b7c7b4-bbea-421f-97dd-ae57e6f82cdb"}]},"item_language":{"attribute_name":"言語","attribute_value_mlt":[{"subitem_language":"eng"}]},"item_resource_type":{"attribute_name":"資源タイプ","attribute_value_mlt":[{"resourcetype":"journal article","resourceuri":"http://purl.org/coar/resource_type/c_6501"}]},"item_title":"A dipeptidyl peptidase-4 inhibitor ameliorates hypertensive cardiac remodeling via angiotensin-II/sodium-proton pump exchanger-1 axis","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"A dipeptidyl peptidase-4 inhibitor ameliorates hypertensive cardiac remodeling via angiotensin-II/sodium-proton pump exchanger-1 axis","subitem_title_language":"en"}]},"item_type_id":"10","owner":"1","path":["501"],"pubdate":{"attribute_name":"PubDate","attribute_value":"2016-12-15"},"publish_date":"2016-12-15","publish_status":"0","recid":"23018","relation_version_is_last":true,"title":["A dipeptidyl peptidase-4 inhibitor ameliorates hypertensive cardiac remodeling via angiotensin-II/sodium-proton pump exchanger-1 axis"],"weko_creator_id":"1","weko_shared_id":-1},"updated":"2023-01-16T04:12:37.667101+00:00"}