Metformin regulates oxLDL-facilitated endothelial dysfunction by modulation of SIRT1 through repressing LOX-1-modulated oxidative signaling

Ching Hsia Hung; Shih Hung Chan; Pei Ming Chu; Huei Chen Lin; Kun Ling Tsai

doi:10.18632/oncotarget.7387

Metformin regulates oxLDL-facilitated endothelial dysfunction by modulation of SIRT1 through repressing LOX-1-modulated oxidative signaling

Ching Hsia Hung, Shih Hung Chan, Pei Ming Chu, Huei Chen Lin, Kun Ling Tsai

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24 Citations (Scopus)

Abstract

It is suggested that oxLDL is decisive in the initiation and development of atherosclerotic injuries. The up-regulation of oxidative stress and the generation of ROS act as key modulators in developing pro-atherosclerotic and anti-atherosclerotic processes in the human endothelial wall. In this present study, we confirmed that metformin enhanced SIRT1 and AMPK expression in human umbilical vein endothelial cells (HUVECs). Metformin also inhibited oxLDL-increased LOX-1 expression and oxLDL-collapsed AKT/eNOS levels. However, silencing SIRT1 and AMPK diminished the protective function of metformin against oxidative injuries. These results provide a new insight regarding the possible molecular mechanisms of metformin.

Original language	English
Pages (from-to)	10773-10787
Number of pages	15
Journal	Oncotarget
Volume	7
Issue number	10
DOIs	https://doi.org/10.18632/oncotarget.7387
Publication status	Published - 2016

All Science Journal Classification (ASJC) codes

Oncology

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10.18632/oncotarget.7387

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title = "Metformin regulates oxLDL-facilitated endothelial dysfunction by modulation of SIRT1 through repressing LOX-1-modulated oxidative signaling",

abstract = "It is suggested that oxLDL is decisive in the initiation and development of atherosclerotic injuries. The up-regulation of oxidative stress and the generation of ROS act as key modulators in developing pro-atherosclerotic and anti-atherosclerotic processes in the human endothelial wall. In this present study, we confirmed that metformin enhanced SIRT1 and AMPK expression in human umbilical vein endothelial cells (HUVECs). Metformin also inhibited oxLDL-increased LOX-1 expression and oxLDL-collapsed AKT/eNOS levels. However, silencing SIRT1 and AMPK diminished the protective function of metformin against oxidative injuries. These results provide a new insight regarding the possible molecular mechanisms of metformin.",

author = "Hung, {Ching Hsia} and Chan, {Shih Hung} and Chu, {Pei Ming} and Lin, {Huei Chen} and Tsai, {Kun Ling}",

note = "Funding Information: This study was supported by grants from the Ministry of Science and Technology (MOST-103-2320-B-006-050) and National Cheng Kung University (NSC 100-2314-B-039-017-MY3, MOST 103-2320-B-006-050, and D103-35A13) and CMU103-N-14, CMU104-N-02.",

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AU - Hung, Ching Hsia

AU - Chan, Shih Hung

AU - Chu, Pei Ming

AU - Lin, Huei Chen

AU - Tsai, Kun Ling

N1 - Funding Information: This study was supported by grants from the Ministry of Science and Technology (MOST-103-2320-B-006-050) and National Cheng Kung University (NSC 100-2314-B-039-017-MY3, MOST 103-2320-B-006-050, and D103-35A13) and CMU103-N-14, CMU104-N-02.

PY - 2016

Y1 - 2016

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AB - It is suggested that oxLDL is decisive in the initiation and development of atherosclerotic injuries. The up-regulation of oxidative stress and the generation of ROS act as key modulators in developing pro-atherosclerotic and anti-atherosclerotic processes in the human endothelial wall. In this present study, we confirmed that metformin enhanced SIRT1 and AMPK expression in human umbilical vein endothelial cells (HUVECs). Metformin also inhibited oxLDL-increased LOX-1 expression and oxLDL-collapsed AKT/eNOS levels. However, silencing SIRT1 and AMPK diminished the protective function of metformin against oxidative injuries. These results provide a new insight regarding the possible molecular mechanisms of metformin.

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Metformin regulates oxLDL-facilitated endothelial dysfunction by modulation of SIRT1 through repressing LOX-1-modulated oxidative signaling

Abstract

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