Endothelial dysfunction promotes the transition from compensatory renal hypertrophy to kidney injury after unilateral nephrectomy in mice.
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Infiltration of M1, but not M2, macrophages is impaired after unilateral ureter obstruction in Nrf2-deficient mice.Direct sGC activation bypasses NO scavenging reactions of intravascular free oxy-hemoglobin and limits vasoconstriction.Nitric oxide in afferent arterioles after uninephrectomy depends on extracellular L-arginine.Distant effects of unilateral renal ischemia/reperfusion on contralateral kidney but not lung in rats: the roles of ROS and iNOS.Metformin attenuates albumin-induced alterations in renal tubular cells in vitro.
P2860
Endothelial dysfunction promotes the transition from compensatory renal hypertrophy to kidney injury after unilateral nephrectomy in mice.
description
2012 nî lūn-bûn
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2012年の論文
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2012年学术文章
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2012年学术文章
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2012年学术文章
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2012年学术文章
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2012年学术文章
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2012年學術文章
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2012年學術文章
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2012年學術文章
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name
Endothelial dysfunction promot ...... nilateral nephrectomy in mice.
@en
Endothelial dysfunction promot ...... nilateral nephrectomy in mice.
@nl
type
label
Endothelial dysfunction promot ...... nilateral nephrectomy in mice.
@en
Endothelial dysfunction promot ...... nilateral nephrectomy in mice.
@nl
prefLabel
Endothelial dysfunction promot ...... nilateral nephrectomy in mice.
@en
Endothelial dysfunction promot ...... nilateral nephrectomy in mice.
@nl
P2093
P2860
P1476
Endothelial dysfunction promot ...... nilateral nephrectomy in mice.
@en
P2093
Hajime Nagasu
Kengo Kidokoro
Minoru Satoh
Naoki Kashihara
Tamaki Sasaki
Yuko Nishi
P2860
P304
P356
10.1152/AJPRENAL.00459.2011
P577
2012-02-29T00:00:00Z