Maternal inflammation activated ROS-p38 MAPK predisposes offspring to heart damages caused by isoproterenol via augmenting ROS generation.
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Sustained elevation of NF-κB activity sensitizes offspring of maternal inflammation to hypertension via impairing PGC-1α recovery.Profiling analysis of long non-coding RNAs in early postnatal mouse hearts.Transforming Growth Factor-β Receptor III is a Potential Regulator of Ischemia-Induced Cardiomyocyte Apoptosis.Inhibitory effect of ethanol extract of Nannochloropsis oceanica on lipopolysaccharide-induced neuroinflammation, oxidative stress, amyloidogenesis and memory impairment.Neferine ameliorates cardiomyoblast apoptosis induced by doxorubicin: possible role in modulating NADPH oxidase/ROS-mediated NFκB redox signaling cascade.miR-155 regulates high glucose-induced cardiac fibrosis via the TGF-β signaling pathway.Prenatal Lipopolysaccharide Exposure Promotes Dyslipidemia in the Male Offspring Rats.
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Maternal inflammation activated ROS-p38 MAPK predisposes offspring to heart damages caused by isoproterenol via augmenting ROS generation.
description
article científic
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article scientifique
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articolo scientifico
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artigo científico
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bilimsel makale
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scientific article published on 22 July 2016
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
Maternal inflammation activate ...... via augmenting ROS generation.
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Maternal inflammation activate ...... via augmenting ROS generation.
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type
label
Maternal inflammation activate ...... via augmenting ROS generation.
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Maternal inflammation activate ...... via augmenting ROS generation.
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Maternal inflammation activate ...... via augmenting ROS generation.
@en
Maternal inflammation activate ...... via augmenting ROS generation.
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P356
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Maternal inflammation activate ...... via augmenting ROS generation.
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Fangjie Wang
Guorong Dan
Hongqin Luo
Jianhua Yu
Jianxiang Zhang
Liangqi Gu
Michael Namaka
P2860
P2888
P356
10.1038/SREP30146
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P577
2016-07-22T00:00:00Z
P6179
1007172991