HADC regulates the diabetic vascular endothelial dysfunction by targetting MnSOD

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HADC regulates the diabetic vascular endothelial dysfunction by targetting MnSOD

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im Oktober 2018 veröffentlichter wissenschaftlicher Artikel

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wetenschappelijk artikel

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наукова стаття, опублікована в жовтні 2018

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HADC regulates the diabetic vascular endothelial dysfunction by targetting MnSOD

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HADC regulates the diabetic vascular endothelial dysfunction by targetting MnSOD

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HADC regulates the diabetic vascular endothelial dysfunction by targetting MnSOD

@en

HADC regulates the diabetic vascular endothelial dysfunction by targetting MnSOD

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HADC regulates the diabetic vascular endothelial dysfunction by targetting MnSOD

@en

HADC regulates the diabetic vascular endothelial dysfunction by targetting MnSOD

@nl

P1476

HADC regulates the diabetic vascular endothelial dysfunction by targetting MnSOD

@en

P2093

Jiao Quan

http://www.w3.org/2001/XMLSchema#string

Ke Hu

http://www.w3.org/2001/XMLSchema#string

Qian Hou

http://www.w3.org/2001/XMLSchema#string

Xiaofeng Liu

http://www.w3.org/2001/XMLSchema#string

Zehao Liu

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P2860

SIRT1 promotes proliferation and prevents senescence through targeting LKB1 in primary porcine aortic endothelial cells

HDAC2 negatively regulates memory formation and synaptic plasticity.

Hdac2 regulates the cardiac hypertrophic response by modulating Gsk3 beta activity

Histone deacetylase-2 is a key regulator of diabetes- and transforming growth factor-beta1-induced renal injury

Mitochondria, endothelial cell function, and vascular diseases.

HDAC2 attenuates TRAIL-induced apoptosis of pancreatic cancer cells.

Long-term administration of the histone deacetylase inhibitor vorinostat attenuates renal injury in experimental diabetes through an endothelial nitric oxide synthase-dependent mechanism

The involvement of NFAT transcriptional activity suppression in SIRT1-mediated inhibition of COX-2 expression induced by PMA/Ionomycin.

Endothelial Dysfunction in Human Diabetes Is Mediated by Wnt5a-JNK Signaling.

HDAC2 blockade by nitric oxide and histone deacetylase inhibitors reveals a common target in Duchenne muscular dystrophy treatment.

P304

BSR20181042

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P31

scholarly article

P356

10.1042/BSR20181042

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P407

English

P433

http://www.w3.org/2001/XMLSchema#string

P478

http://www.w3.org/2001/XMLSchema#string

P577

2018-10-31T00:00:00Z

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P698

30217947

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P921

Biofiseg

molecular biology

P932

6165838

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