| pubmed-article:17562700 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17562700 | lifeskim:mentions | umls-concept:C0225828 | lld:lifeskim |
| pubmed-article:17562700 | lifeskim:mentions | umls-concept:C1521761 | lld:lifeskim |
| pubmed-article:17562700 | lifeskim:mentions | umls-concept:C0311404 | lld:lifeskim |
| pubmed-article:17562700 | lifeskim:mentions | umls-concept:C2611952 | lld:lifeskim |
| pubmed-article:17562700 | lifeskim:mentions | umls-concept:C0205164 | lld:lifeskim |
| pubmed-article:17562700 | pubmed:issue | 32 | lld:pubmed |
| pubmed-article:17562700 | pubmed:dateCreated | 2007-8-6 | lld:pubmed |
| pubmed-article:17562700 | pubmed:abstractText | An inexorable loss of terminally differentiated heart muscle cells is a crucial causal factor for heart failure. Here, we have provided several lines of evidence to demonstrate that mitofusin-2 (Mfn-2; also called hyperplasia suppressor gene), a member of the mitofusin family, is a major determinant of oxidative stress-mediated cardiomyocyte apoptosis. First, oxidative stress with H(2)O(2) led to concurrent increases in Mfn-2 expression and apoptosis in cultured neonatal rat cardiomyocytes. Second, overexpression of Mfn-2 to a level similar to that induced by H(2)O(2) was sufficient to trigger myocyte apoptosis, which is associated with profound inhibition of Akt activation without altering ERK1/2 signaling. Third, Mfn-2 silencing inhibited oxidative stress-induced apoptosis in H9C2 cells, a cardiac muscle cell line. Furthermore, Mfn-2-induced myocyte apoptosis was abrogated by inhibition of caspase-9 (but not caspase-8) and by overexpression of Bcl-x(L) or enhanced activation of phosphatidylinositol 3-kinase-Akt, suggesting that inhibition of Akt signaling and activation of the mitochondrial death pathway are essentially involved in Mfn-2-induced heart muscle cell apoptosis. These results indicate that increased cardiac Mfn-2 expression is both necessary and sufficient for oxidative stress-induced heart muscle cell apoptosis, suggesting that Mfn-2 deregulation may be a crucial pathogenic element and a potential therapeutic target for heart failure. | lld:pubmed |
| pubmed-article:17562700 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17562700 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17562700 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:17562700 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17562700 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17562700 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17562700 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17562700 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17562700 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17562700 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17562700 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:17562700 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:17562700 | pubmed:author | pubmed-author:RoweC TCT | lld:pubmed |
| pubmed-article:17562700 | pubmed:author | pubmed-author:TangJianJ | lld:pubmed |
| pubmed-article:17562700 | pubmed:author | pubmed-author:XiaoRui-PingR... | lld:pubmed |
| pubmed-article:17562700 | pubmed:author | pubmed-author:ChengHepingH | lld:pubmed |
| pubmed-article:17562700 | pubmed:author | pubmed-author:ZhengMingM | lld:pubmed |
| pubmed-article:17562700 | pubmed:author | pubmed-author:ChenKuang-Hue... | lld:pubmed |
| pubmed-article:17562700 | pubmed:author | pubmed-author:CaoChunmeiC | lld:pubmed |
| pubmed-article:17562700 | pubmed:author | pubmed-author:ChenChunleiC | lld:pubmed |
| pubmed-article:17562700 | pubmed:author | pubmed-author:ZhangWanruiW | lld:pubmed |
| pubmed-article:17562700 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17562700 | pubmed:day | 10 | lld:pubmed |
| pubmed-article:17562700 | pubmed:volume | 282 | lld:pubmed |
| pubmed-article:17562700 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17562700 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17562700 | pubmed:pagination | 23354-61 | lld:pubmed |
| pubmed-article:17562700 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:17562700 | pubmed:meshHeading | pubmed-meshheading:17562700... | lld:pubmed |
| pubmed-article:17562700 | pubmed:meshHeading | pubmed-meshheading:17562700... | lld:pubmed |
| pubmed-article:17562700 | pubmed:meshHeading | pubmed-meshheading:17562700... | lld:pubmed |
| pubmed-article:17562700 | pubmed:meshHeading | pubmed-meshheading:17562700... | lld:pubmed |
| pubmed-article:17562700 | pubmed:meshHeading | pubmed-meshheading:17562700... | lld:pubmed |
| pubmed-article:17562700 | pubmed:meshHeading | pubmed-meshheading:17562700... | lld:pubmed |
| pubmed-article:17562700 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17562700 | pubmed:articleTitle | Mitofusin-2 is a major determinant of oxidative stress-mediated heart muscle cell apoptosis. | lld:pubmed |
| pubmed-article:17562700 | pubmed:affiliation | Institute of Cardiovascular Sciences, Peking University, Beijing 100083, China. | lld:pubmed |
| pubmed-article:17562700 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17562700 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:17562700 | pubmed:publicationType | Research Support, N.I.H., Intramural | lld:pubmed |
| entrez-gene:64476 | entrezgene:pubmed | pubmed-article:17562700 | lld:entrezgene |
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