Pim-1 kinase inhibits pathological injury by promoting cardioprotective signaling.
Pim-1 kinase inhibits pathological injury by promoting cardioprotective signaling.
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DOI：
10.1016/j.yjmcc.2011.01.004
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发表时间：
2011-10
影响因子：
5
通讯作者：
Sussman MA
中科院分区：
文献类型：
--
作者：
Fischer KM;Cottage CT;Konstandin MH;Völkers M;Khan M;Sussman MA
干细胞在生物体的整个生命周期中介导组织修复。然而，干细胞减轻灾难性损伤的能力，如严重心肌梗死后持续的损伤，不足以重建心脏和恢复功能能力。然而，利用这些细胞减轻心肌损伤的能力，正在研究各种增强修复机制以改善损伤后心脏结构和功能的方法。这些研究已经导致发现了介导心脏保护和增强内源性修复的各种因子，其通过1）挽救存活的心肌，2）促进干细胞归巢和3）增加损伤部位干细胞群的存活和增殖。在此，我们报告了Akt激酶的下游靶点，命名为Pim-1，其促进心脏保护信号并增强病理损伤后的心脏结构和功能。本文所述的研究汇编支持使用Pim-1来增强病理损伤后的长期心肌修复。
Stem cells mediate tissue repair throughout the lifespan of an organism. However, the ability of stem cells to mitigate catastrophic damage, such as that sustained after major myocardial infarction is inadequate to rebuild the heart and restore functional capacity. However, capitalizing on the ability of these cells to attenuate damage in the myocardium, various maneuvers that enhance repair mechanisms to improve cardiac structure and function after injury are being investigated. These studies have led to discovery of various factors that mediate cardioprotection and enhance endogenous repair by 1) salvaging surviving myocardium, 2) promoting homing of stem cells and 3) increasing survival and proliferation of stem cell populations at the site of injury. Herein we report upon a downstream target of Akt kinase, named Pim-1, which promotes cardioprotective signaling and enhances cardiac structure and function after pathological injury. The compilation of studies presented here supports use of Pim-1 to enhance long-term myocardial repair after pathological damage.
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影响因子：
6
作者：
Chen, Jian;Kobayashi, Masanobu;Lee, Mong-Hong
通讯作者：
Lee, Mong-Hong
影响因子：
1.6
作者：
Bhattacharya, N;Wang, ZP;Magnuson, NS
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影响因子：
2
作者：
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通讯作者：
Sussman MA
影响因子：
2.7
作者：
Bailey B;Izarra A;Alvarez R;Fischer KM;Cottage CT;Quijada P;Díez-Juan A;Sussman MA
通讯作者：
Sussman MA
影响因子：
5.3
作者：
Mikkers, H;Nawijn, M;Berns, A
通讯作者：
Berns, A