Page last updated: 2024-11-04

sb 239063 and Cardiac Hypertrophy

sb 239063 has been researched along with Cardiac Hypertrophy in 1 studies

SB 239063: structure in first source
SB-239063 : A member of the class of imidazoles carrying 4-hydroxycyclohexyl, 4-fluorophenyl and 2-methoxypyrimidin-4-yl substituents at positions 1, 4 and 5 respectively.

Cardiac Hypertrophy: Enlargement of the HEART due to chamber HYPERTROPHY, an increase in wall thickness without an increase in the number of cells (MYOCYTES, CARDIAC). It is the result of increase in myocyte size, mitochondrial and myofibrillar mass, as well as changes in extracellular matrix.

Research Excerpts

ExcerptRelevanceReference
"Numerous pathological mediators of cardiac hypertrophy (eg, neurohormones, cytokines, and stretch) have been shown to activate p38 MAPK."1.31Hypertensive end-organ damage and premature mortality are p38 mitogen-activated protein kinase-dependent in a rat model of cardiac hypertrophy and dysfunction. ( Adams, JL; Angermann, CE; Behr, TM; Brooks, DP; Chandra, S; Coatney, RW; Kumar, S; Lee, JC; Nelson, AH; Nerurkar, SS; Ohlstein, EH; Sackner-Bernstein, JD; Sisko, J; Sulpizio, A; Willette, RN; Woods, TN, 2001)

Research

Studies (1)

TimeframeStudies, this research(%)All Research%
pre-19900 (0.00)18.7374
1990's0 (0.00)18.2507
2000's1 (100.00)29.6817
2010's0 (0.00)24.3611
2020's0 (0.00)2.80

Authors

AuthorsStudies
Behr, TM1
Nerurkar, SS1
Nelson, AH1
Coatney, RW1
Woods, TN1
Sulpizio, A1
Chandra, S1
Brooks, DP1
Kumar, S1
Lee, JC1
Ohlstein, EH1
Angermann, CE1
Adams, JL1
Sisko, J1
Sackner-Bernstein, JD1
Willette, RN1

Other Studies

1 other study available for sb 239063 and Cardiac Hypertrophy

ArticleYear
Hypertensive end-organ damage and premature mortality are p38 mitogen-activated protein kinase-dependent in a rat model of cardiac hypertrophy and dysfunction.
    Circulation, 2001, Sep-11, Volume: 104, Issue:11

    Topics: Animals; Cardiomegaly; Disease Models, Animal; Dose-Response Relationship, Drug; Echocardiography; E

2001