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September 9, 2006AJP Heart and Circulatory Physiology

Chronic NOS inhibition actuates endothelial-mesenchymal transformation

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Population

Tie-2 promoter-driven green fluorescent protein mice and in vitro endothelial cells

Design

Preclinical

Authors

EOEdmond O’RiordanNMNatalia MendelevSPSusann Patschan

Discussion

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Overview

Hypothesis-generating for endothelial-mesenchymal transition in CKD microvascular rarefaction; clinical relevance remains untested.

Structured PICO

P
Population
Tie-2 promoter-driven green fluorescent protein mice and in vitro endothelial cells
I
Intervention
NOS inhibitors (nonhypertensinogenic doses in vivo, asymmetric dimethylarginine in vitro)
O
Outcome
Expression of collagen XVIII/endostatin, capillary rarefaction, and markers of endothelial-mesenchymal transdifferentiationsurrogate

Chronic NOS inhibition induces endothelial-mesenchymal transdifferentiation and profibrotic signaling, providing a mechanism for microvascular rarefaction in chronic kidney disease.

Cite This Study

O’Riordan et al. (2006) studied this question.

synapsesocial.com/papers/6a6fbfa8ac440176ef28695bhttps://doi.org/10.1152/ajpheart.00560.2006
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Also Consider

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  1. 1Nitric oxide inhibition induces early activation of type I collagen gene in renal resistance vessels and glomeruli in transgenic mice. Role of endothelin.1998 · 134 citations
  2. 2Endothelial Dilatory Function Predicts Individual Susceptibility to Renal Damage in the 5/6 Nephrectomized Rat2002 · 60 citations
  3. 3Molecular insights into renal interstitial fibrosis.1996 · 642 citations
  4. 4Increased plasma phenylacetic acid in patients with end-stage renal failure inhibits iNOS expression2003 · 115 citations
  5. 5Vascular Endothelial Cell Regulation of Extracellular Matrix Collagen1998 · 93 citations