Linked Life Data

15030789

Source:http://linkedlifedata.com/resource/pubmed/id/15030789

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2004-3-19
pubmed:abstractText
Activation of stress-activated mitogen-activated protein kinases (SAPKs), mainly c-Jun N-terminal kinase (JNK) and p38, have long been associated with different forms of cardiac pathology across a wide spectrum of species. However, their specific roles in the development of heart failure are still unclear. Previous studies in neonatal myocytes in culture suggest a critical role for both JNK and p38 in hypertrophy and apoptosis. A far more complex picture has been provided by recent observations from both cellular and transgenic models that have not only challenged their role in hypertrophy and cell death but have also pointed out novel functions of SAPKs in different aspects of cardiac pathology, including contractile function, extracellular matrix remodeling, intercellular communication, and metabolic regulation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1050-1738
pubmed:author
pubmed:issnType
Print
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
50-5
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Stress-activated MAP kinases in cardiac remodeling and heart failure; new insights from transgenic studies.
pubmed:affiliation
Division of Molecular Medicine, Departments of Anesthesiology and Medicine, University of California at Los Angeles, Los Angeles, California 90095, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, Non-U.S. Gov't