Abstract:
:In humans injured myocardium cannot avert the onset and progression of ventricular dysfunction because of limited regenerative ability of myocytes. Although limited renaissance of cardiomyocytes has been reported in human infarcted hearts, it is generally accredited that non-functional fibrous tissue replaces the dead myocardium. High cardiovascular morbidity and dearth of donor hearts warrant a constant hunt for radically different approach to treat heart failure. Pluripotent stem (PS) cells possess the ability to produce functional cardiomyocytes for clinical applications and drug development, which may provide the answer to this problem. Although progress has been made in differentiating human PS cells into cardiomyocytes, however, the in vitro differentiation of pluripotent cells into cardiomyocytes involves a poorly defined, inefficient and relatively non-selective process. A thorough understanding of signaling pathways would tender a roadmap for the streamlined development of in vitro cardiac differentiation strategies. The ability to obtain unlimited numbers of human cardiomyocytes would improve development of cell-based therapies for cardiovascular diseases, facilitate the study of cardiovascular biology and improve the early stages of drug discovery. Here in this review, we highlight the interacting endogenous cellular signals and their modulators involved in directing the human PSCs towards cardiac differentiation.
journal_name
Cell Signaljournal_title
Cellular signallingauthors
Verma V,Purnamawati K,Manasi,Shim Wdoi
10.1016/j.cellsig.2013.01.027subject
Has Abstractpub_date
2013-05-01 00:00:00pages
1096-107issue
5eissn
0898-6568issn
1873-3913pii
S0898-6568(13)00041-7journal_volume
25pub_type
杂志文章,评审abstract::In this study, we showed that nitric oxide (NO) donors induced the mesangial cell proliferation and cyclooxygenase-2 (COX-2) protein expression in murine mesangial cells. An inflammatory condition [lipopolysaccharide (LPS) plus interferon-gamma (IFN-gamma)] could also induce cell proliferation and significantly enhanc...
journal_title:Cellular signalling
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/0898-6568(94)00041-7
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journal_title:Cellular signalling
pub_type: 杂志文章,评审
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journal_title:Cellular signalling
pub_type: 杂志文章,评审
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journal_title:Cellular signalling
pub_type: 杂志文章
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2015.03.024
更新日期:2015-07-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2010.11.007
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2007.08.013
更新日期:2007-12-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/0898-6568(90)90045-c
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2017.04.009
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journal_title:Cellular signalling
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pub_type: 杂志文章
doi:10.1016/0898-6568(94)90023-x
更新日期:1994-11-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2009.09.039
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2015.03.001
更新日期:2015-06-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2007.01.010
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pub_type: 杂志文章
doi:10.1016/j.cellsig.2008.05.017
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2008.06.013
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journal_title:Cellular signalling
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