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心脏核高迁移率族蛋白盒1通过抑制DNA损伤反应改善病理性心脏肥大。

Cardiac Nuclear High-Mobility Group Box 1 Ameliorates Pathological Cardiac Hypertrophy by Inhibiting DNA Damage Response.

作者信息

Takahashi Tetsuya, Shishido Tetsuro, Kinoshita Daisuke, Watanabe Ken, Toshima Taku, Sugai Takayuki, Narumi Taro, Otaki Yoichiro, Tamura Harutoshi, Nishiyama Satoshi, Arimoto Takanori, Takahashi Hiroki, Miyamoto Takuya, Watanabe Tetsu, Woo Chang-Hoon, Abe Jun-Ichi, Takeishi Yasuchika, Kubota Isao, Watanabe Masafumi

机构信息

Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.

Department of Pharmacology, College of Medicine, Yeungnam University, Daegu, Republic of Korea.

出版信息

JACC Basic Transl Sci. 2019 Apr 29;4(2):234-247. doi: 10.1016/j.jacbts.2018.11.011. eCollection 2019 Apr.

DOI:10.1016/j.jacbts.2018.11.011
PMID:31061925
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6488753/
Abstract

High-mobility group box 1 (HMGB1) is a deoxyribonucleic acid (DNA)-binding protein associated with DNA repair. Decreased nuclear HMGB1 expression and increased DNA damage response (DDR) were observed in human failing hearts. DNA damage and DDR as well as cardiac remodeling were suppressed in cardiac-specific HMGB1 overexpression transgenic mice after angiotensin II stimulation as compared with wild-type mice. In vitro, inhibition of HMGB1 increased phosphorylation of extracellular signal-related kinase 1/2 and nuclear factor kappa B, which was rescued by DDR inhibitor treatment. DDR inhibitor treatment provided a cardioprotective effect on angiotensin II-induced cardiac remodeling in mice.

摘要

高迁移率族蛋白B1（HMGB1）是一种与DNA修复相关的脱氧核糖核酸（DNA）结合蛋白。在人类衰竭心脏中观察到核内HMGB1表达降低以及DNA损伤反应（DDR）增加。与野生型小鼠相比，血管紧张素II刺激后，心脏特异性HMGB1过表达转基因小鼠的DNA损伤、DDR以及心脏重塑受到抑制。在体外，抑制HMGB1会增加细胞外信号调节激酶1/2和核因子κB的磷酸化，DDR抑制剂处理可使其恢复。DDR抑制剂处理对小鼠血管紧张素II诱导的心脏重塑具有心脏保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aced/6488753/ea86a4123129/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aced/6488753/14456b188f61/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aced/6488753/474689dc3744/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aced/6488753/2c7e267c91e9/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aced/6488753/d24fbb0cf6d7/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aced/6488753/e81b18cb9174/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aced/6488753/11da954e18fc/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aced/6488753/466fea133260/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aced/6488753/ea86a4123129/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aced/6488753/14456b188f61/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aced/6488753/474689dc3744/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aced/6488753/2c7e267c91e9/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aced/6488753/d24fbb0cf6d7/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aced/6488753/e81b18cb9174/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aced/6488753/11da954e18fc/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aced/6488753/466fea133260/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aced/6488753/ea86a4123129/gr7.jpg

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