August 1, 2002HypertensionOpen Access

N -Acetyl-Ser-Asp-Lys-Pro Inhibits Phosphorylation of Smad2 in Cardiac Fibroblasts

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Population

Isolated rat cardiac fibroblasts and vascular smooth muscle cells

Comparison

N-Acetyl-Ser-Asp-Lys-Pro (AcSDKP) vs Untreated control (implied)

Design

Preclinical

Authors

SPSaraswati PokharelRoswell Park Comprehensive Cancer Center SRSaman RasoulÇevre ve Şehircilik Bakanlığı ARAnton J.M. RoksErasmus MC

Discussion

Member takes

Implication

AcSDKP effects in fibroblasts are hypothesis-generating; leaves open any role in ACE inhibitor antifibrosis in patients.

Structured PICO

Population

Isolated rat cardiac fibroblasts and vascular smooth muscle cells

Intervention

N-Acetyl-Ser-Asp-Lys-Pro (AcSDKP)

Comparator

Untreated control (implied)

Outcome

Cell proliferation and TGFbeta1-mediated Smad signaling (Smad2 phosphorylation and nuclear translocation)surrogate

AcSDKP inhibits cardiac fibroblast growth and TGFbeta1-stimulated Smad2 phosphorylation, suggesting a novel angiotensin II-independent mechanism by which ACE inhibitors may reduce cardiac fibrosis.

Cite This Study

Pokharel et al. (2002) studied this question.

synapsesocial.com/papers/6a852c109df997f4bbd69f8e https://doi.org/10.1161/01.hyp.0000025880.56816.fa

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N -Acetyl-Ser-Asp-Lys-Pro Inhibits Phosphorylation of Smad2 in Cardiac Fibroblasts

Discussion

Member takes

Implication

Structured PICO

Cite This Study

N -Acetyl-Ser-Asp-Lys-Pro Inhibits Phosphorylation of Smad2 in Cardiac Fibroblasts

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider