rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
4
|
pubmed:dateCreated |
2010-2-11
|
pubmed:abstractText |
Proliferation of mammalian cardiomyocytes stops during the first weeks after birth, preventing the heart from regenerating after injury. Recently, several studies have indicated that induction of cardiomyocyte proliferation can be utilized to regenerate the mammalian heart. Thus, it is important to identify novel factors that can induce proliferation of cardiomyocytes. Here, we determine the effect of TNF-related weak inducer of apoptosis (TWEAK) on cardiomyocytes, a cytokine known to regulate proliferation in several other cell types.
|
pubmed:commentsCorrections |
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Apoptosis Regulatory Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Ccnd2 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclin D2,
http://linkedlifedata.com/resource/pubmed/chemical/Ki-67 Antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Small Interfering,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor,
http://linkedlifedata.com/resource/pubmed/chemical/TWEAK protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/TWEAK receptor,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factors
|
pubmed:status |
MEDLINE
|
pubmed:month |
Mar
|
pubmed:issn |
1755-3245
|
pubmed:author |
|
pubmed:issnType |
Electronic
|
pubmed:day |
1
|
pubmed:volume |
85
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
681-90
|
pubmed:meshHeading |
pubmed-meshheading:19887380-Animals,
pubmed-meshheading:19887380-Animals, Newborn,
pubmed-meshheading:19887380-Apoptosis Regulatory Proteins,
pubmed-meshheading:19887380-Cell Division,
pubmed-meshheading:19887380-Cells, Cultured,
pubmed-meshheading:19887380-Cyclin D2,
pubmed-meshheading:19887380-Female,
pubmed-meshheading:19887380-Gene Expression,
pubmed-meshheading:19887380-Ki-67 Antigen,
pubmed-meshheading:19887380-Membrane Proteins,
pubmed-meshheading:19887380-Mitosis,
pubmed-meshheading:19887380-Myocytes, Cardiac,
pubmed-meshheading:19887380-Pregnancy,
pubmed-meshheading:19887380-RNA, Small Interfering,
pubmed-meshheading:19887380-Rats,
pubmed-meshheading:19887380-Rats, Sprague-Dawley,
pubmed-meshheading:19887380-Receptors, Tumor Necrosis Factor,
pubmed-meshheading:19887380-Regeneration,
pubmed-meshheading:19887380-Signal Transduction,
pubmed-meshheading:19887380-Tumor Necrosis Factors
|
pubmed:year |
2010
|
pubmed:articleTitle |
TWEAK is a positive regulator of cardiomyocyte proliferation.
|
pubmed:affiliation |
Department of Cardiac Development and Remodelling, Excellence Cluster Cardio-Pulmonary System, Max Planck Institute for Heart and Lung Research, Parkstrasse 1, Bad Nauheim 61231, Germany.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|