miR-106a promotes cardiac hypertrophy by targeting mitofusin 2. (Q32872171)

11 July 2017

title

miR-106a promotes cardiac hypertrophy by targeting mitofusin 2. (English)

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11 July 2017

Xiaoxiang Guan

1

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11 July 2017

Lu Wang

2

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11 July 2017

Zhenhong Liu

3

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11 July 2017

Xiaofei Guo

4

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11 July 2017

Yuan Jiang

5

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11 July 2017

Ying Lu

6

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11 July 2017

Yanli Peng

7

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11 July 2017

Tianhua Liu

8

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11 July 2017

Baofeng Yang

9

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11 July 2017

Hongli Shan

10

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11 July 2017

Yong Zhang

11

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11 July 2017

Chaoqian Xu

12

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11 July 2017

publication date

23 August 2016

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Journal of Molecular and Cellular Cardiology

11 July 2017

published in

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11 July 2017

volume

99

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11 July 2017

page(s)

207-217

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11 July 2017

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A Mitofusin-2-dependent inactivating cleavage of Opa1 links changes in mitochondria cristae and ER contacts in the postprandial liver.

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Mitofusin 2 triggers vascular smooth muscle cell apoptosis via mitochondrial death pathway

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Mitofusins 1 and 2 are essential for postnatal metabolic remodeling in heart

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Central role of mitofusin 2 in autophagosome-lysosome fusion in cardiomyocytes

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Scutellarin alleviates interstitial fibrosis and cardiac dysfunction of infarct rats by inhibiting TGFβ1 expression and activation of p38‐MAPK and ERK1/2

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Downregulation of miR-133 via MAPK/ERK signaling pathway involved in nicotine-induced cardiomyocyte apoptosis

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Mitofusin 1 and 2 play distinct roles in mitochondrial fusion reactions via GTPase activity

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miR-106a represses the Rb tumor suppressor p130 to regulate cellular proliferation and differentiation in high-grade serous ovarian carcinoma.

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Identifiers

DOI

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11 July 2017

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