November 12, 2004Circulation Research
Transforming Growth Factor β Receptor Endoglin Is Expressed in Cardiac Fibroblasts and Modulates Profibrogenic Actions of Angiotensin II
Key result
Angiotensin II upregulated endoglin expression in cardiac fibroblasts via the AT1 receptor, modulating profibrotic effects including decreased MMP-1 and increased type I collagen expression.
Population
Cardiac fibroblasts (CF) from adult Sprague Dawley rats
Comparison
Angiotensin II exposure, with or without AT1… vs Control/quiescent cardiac fibroblasts or Ang II…
Design
Preclinical
Authors
Discussion
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Member takes
Implication
May identify endoglin as antifibrotic target in Ang II remodeling; leaves open clinical translation pending human studies.
Structured PICO
P
Population
In vitro experiments using cardiac fibroblasts from adult Sprague Dawley rats to study Angiotensin II-induced myocardial fibrosis.
I
Intervention
Angiotensin II (Ang II) exposure, with or without AT1 receptor antagonists (valsartan, candesartan, losartan), AT2 receptor antagonist (PD123319), MAPKp42/44 inhibition, or specific endoglin antibody
C
Comparator
Control/quiescent cardiac fibroblasts or Ang II alone
O
Outcome
Expression of endoglin mRNA and protein, MMP-1 protein expression, and type I collagen protein expressionsurrogate
Endoglin is upregulated in cardiac fibroblasts by Angiotensin II via the AT1 receptor, modulating its profibrotic effects and providing novel insights into cardiac remodeling.
Cite This Study
Chen et al. (2004) studied Myocardial fibrosis. Angiotensin II vs. Quiescent cardiac fibroblasts was evaluated on Endoglin mRNA and protein expression, MMP-1 and type I collagen expression. Angiotensin II upregulated endoglin expression in cardiac fibroblasts via the AT1 receptor, modulating profibrotic effects including decreased MMP-1 and increased type I collagen expression.