Lysosomal cysteine peptidase cathepsin l protects against cardiac hypertrophy through blocking akt/gsk3 beta signaling
文献类型：期刊论文
| 作者 | Tang, Qizhu1,2; Cai, Jun3,4; Shen, Difei1,2; Bian, Zhouyan1,2; Yan, Ling1,2; Wang, You-Xin5,6; Lan, Jie5,6; Zhuang, Guo-Qing5,6; Ma, Wen-Zhan5,6; Wang, Wei5,6 |
| 刊名 | Journal of molecular medicine-jmm
 |
| 出版日期 | 2009-03-01 |
| 卷号 | 87期号:3页码:249-260 |
| 关键词 | Cathepsin l Cardiac remodeling Akt Fibrosis Gsk3 beta |
| ISSN号 | 0946-2716 |
| DOI | 10.1007/s00109-008-0423-2 |
| 通讯作者 | Tang, qizhu(qizhu.tang@ymail.com) |
| 英文摘要 | The lysosomal cysteine peptidase cathepsin l (ctsl) is an important lysosomal proteinase involved in a variety of cellular functions including intracellular protein turnover, epidermal homeostasis, and hair development. deficiency of ctsl in mice results in a progressive dilated cardiomyopathy. in the present study, we tested the hypothesis that cardiac overexpression of human ctsl in the murine heart would protect against cardiac hypertrophy in vivo. the effects of constitutive human ctsl expression on cardiac hypertrophy were investigated using in vitro and in vivo models. cardiac hypertrophy was produced by aortic banding (ab) in ctsl transgenic mice and control animals. the extent of cardiac hypertrophy was quantitated by two-dimensional and m-mode echocardiography as well as by molecular and pathological analyses of heart samples. constitutive overexpression of human ctsl in the murine heart attenuated the hypertrophic response, markedly reduced apoptosis, and fibrosis. cardiac function was also preserved in hearts with increased ctsl levels in response to hypertrophic stimuli. these beneficial effects were associated with attenuation of the akt/gsk3 beta signaling cascade. our in vitro studies further confirmed that ctsl expression in cardiomyocytes blunts cardiac hypertrophy through blocking of akt/gsk3 beta signaling. the study indicates that ctsl improves cardiac function and inhibits cardiac hypertrophy, inflammation, and fibrosis through blocking akt/gsk3 beta signaling. |
| WOS关键词 | MICE DEFICIENT ; KNOCKOUT MICE ; DISEASE ; HEART ; PROTEASES ; PATHWAYS ; CARDIOMYOPATHY ; APOPTOSIS ; TARGETS ; CANCER |
| WOS研究方向 | Genetics & Heredity ; Research & Experimental Medicine |
| WOS类目 | Genetics & Heredity ; Medicine, Research & Experimental |
| 语种 | 英语 |
| WOS记录号 | WOS:000263502100004 |
| 出版者 | SPRINGER |
| URI标识 | http://www.irgrid.ac.cn/handle/1471x/2394832 |
| 专题 | 中国科学院大学 |
| 通讯作者 | Tang, Qizhu |
| 作者单位 | 1.Wuhan Univ, Cardiovasc Res Inst, Wuhan 430060, Peoples R China 2.Wuhan Univ, Renmin Hosp, Dept Cardiol, Wuhan 430060, Peoples R China 3.Harvard Univ, Massachusetts Gen Hosp, Sch Med, Cardiovasc Res Ctr, Boston, MA 02129 USA 4.Capital Med Univ, Beijing Chaoyang Hosp, Dept Cardiol, Beijing 100020, Peoples R China 5.Chinese Acad Sci, Grad Sch, Beijing 100049, Peoples R China 6.Capital Med Univ, Sch Publ Hlth & Family Med, Beijing 100069, Peoples R China |
| 推荐引用方式 GB/T 7714 | Tang, Qizhu,Cai, Jun,Shen, Difei,et al. Lysosomal cysteine peptidase cathepsin l protects against cardiac hypertrophy through blocking akt/gsk3 beta signaling[J]. Journal of molecular medicine-jmm,2009,87(3):249-260. |
| APA | Tang, Qizhu.,Cai, Jun.,Shen, Difei.,Bian, Zhouyan.,Yan, Ling.,...&Wang, Wei.(2009).Lysosomal cysteine peptidase cathepsin l protects against cardiac hypertrophy through blocking akt/gsk3 beta signaling.Journal of molecular medicine-jmm,87(3),249-260. |
| MLA | Tang, Qizhu,et al."Lysosomal cysteine peptidase cathepsin l protects against cardiac hypertrophy through blocking akt/gsk3 beta signaling".Journal of molecular medicine-jmm 87.3(2009):249-260. |
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来源：中国科学院大学
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