| http://purl.uniprot.org/citations/29052864 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/29052864 | http://www.w3.org/2000/01/rdf-schema#comment | "Hypertension-stimulated cardiac hypertrophy and apoptosis play critical roles in the progression of heart failure. Our previous study suggested that hypertensive angiotensin II (Ang II) enhanced insulin-like growth factor receptor II (IGF-IIR) expression and cardiomyocyte apoptosis, which are involved JNK activation, sirtuin1 (SIRT1) degradation, and heat-shock transcription factor 1 (HSF1) acetylation. Moreover, previous studies have implied that short-term hypoxia (STH) might exert cardioprotective effects. However, the effects of STH on Ang II-induced cardiomyocyte apoptosis remain unknown. In this study, we found that STH reduced myocardial apoptosis caused by Ang II via upregulation of the Mas receptor (MasR) to inhibit the AT1 R signaling pathway. STH activates MasR to counteract the Ang II pro-apoptotic signaling cascade by inhibiting IGF-IIR expression via downregulation of JNK activation and reduction of SIRT1 degradation. Hence, HSF could remain deacetylated, and repress IGF-IIR expression. These effects decrease the activation of downstream pro-apoptotic and hypertrophic cascades and protect cardiomyocytes from Ang II-induced injury. In addition, we also found that silencing MasR expression enhanced Ang II-induced cardiac hypertrophy and the apoptosis signaling pathway. These findings suggest a critical role for MasR in cardiomyocyte survival. Altogether, our findings indicate that STH protects cardiomyocytes from Ang II-stimulated apoptosis. The protective effects of STH are associated with the upregulation of MasR to inhibit AT1 R signaling. STH could be a potential therapeutic strategy for cardiac diseases in hypertensive patients."xsd:string |
| http://purl.uniprot.org/citations/29052864 | http://purl.org/dc/terms/identifier | "doi:10.1002/jcb.26440"xsd:string |
| http://purl.uniprot.org/citations/29052864 | http://purl.uniprot.org/core/author | "Huang C.Y."xsd:string |
| http://purl.uniprot.org/citations/29052864 | http://purl.uniprot.org/core/author | "Lin J.W."xsd:string |
| http://purl.uniprot.org/citations/29052864 | http://purl.uniprot.org/core/author | "Chang C.F."xsd:string |
| http://purl.uniprot.org/citations/29052864 | http://purl.uniprot.org/core/author | "Li J.C."xsd:string |
| http://purl.uniprot.org/citations/29052864 | http://purl.uniprot.org/core/author | "Viswanadha V.P."xsd:string |
| http://purl.uniprot.org/citations/29052864 | http://purl.uniprot.org/core/author | "Day C.H."xsd:string |
| http://purl.uniprot.org/citations/29052864 | http://purl.uniprot.org/core/author | "Chang T.T."xsd:string |
| http://purl.uniprot.org/citations/29052864 | http://purl.uniprot.org/core/author | "Cheng S.M."xsd:string |
| http://purl.uniprot.org/citations/29052864 | http://purl.uniprot.org/core/author | "Ho T.J."xsd:string |
| http://purl.uniprot.org/citations/29052864 | http://purl.uniprot.org/core/author | "Chang R.L."xsd:string |
| http://purl.uniprot.org/citations/29052864 | http://purl.uniprot.org/core/author | "Ju D.T."xsd:string |
| http://purl.uniprot.org/citations/29052864 | http://purl.uniprot.org/core/date | "2018"xsd:gYear |
| http://purl.uniprot.org/citations/29052864 | http://purl.uniprot.org/core/name | "J Cell Biochem"xsd:string |
| http://purl.uniprot.org/citations/29052864 | http://purl.uniprot.org/core/pages | "2742-2749"xsd:string |
| http://purl.uniprot.org/citations/29052864 | http://purl.uniprot.org/core/title | "Short-term hypoxia upregulated Mas receptor expression to repress the AT1 R signaling pathway and attenuate Ang II-induced cardiomyocyte apoptosis."xsd:string |
| http://purl.uniprot.org/citations/29052864 | http://purl.uniprot.org/core/volume | "119"xsd:string |
| http://purl.uniprot.org/citations/29052864 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/29052864 |
| http://purl.uniprot.org/citations/29052864 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/29052864 |
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| http://purl.uniprot.org/uniprot/#_D3DNG8-mappedCitation-29052864 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29052864 |
| http://purl.uniprot.org/uniprot/#_P04201-mappedCitation-29052864 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29052864 |
| http://purl.uniprot.org/uniprot/#_Q13063-mappedCitation-29052864 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29052864 |