|本期目录/Table of Contents|

[1]聂雅琴,乌日娜,金慧,等.高迁移率族蛋白1通过调控自噬因子P62调节心肌细胞纤维化[J].国际心血管病杂志,2024,02:109-113.
 NIE Yaqin,WU Rina,JIN Hui,et al.HMGB1 induces myocardial fibrosis by regulating autophagy factor P62[J].International Journal of Cardiovascular Disease,2024,02:109-113.
点击复制

高迁移率族蛋白1通过调控自噬因子P62调节心肌细胞纤维化(PDF)

《国际心血管病杂志》[ISSN:1006-6977/CN:61-1281/TN]

期数:
2024年02期
页码:
109-113
栏目:
基础研究
出版日期:
2024-03-25

文章信息/Info

Title:
HMGB1 induces myocardial fibrosis by regulating autophagy factor P62
作者:
聂雅琴乌日娜金慧张广平李永明智利薛仕煊娜日格乐
014040 包头医学院中心临床医学院(聂雅琴);014040 包头市中心医院心血管内科(乌日娜,金慧,张广平, 李永明, 智利, 薛仕煊, 娜日格乐)
Author(s):
NIE Yaqin1 WU Rina2 JIN Hui2 ZHANG Guangping2 LI Yongming2 ZHI Li2 XUE Shixuan2 NARI Gele2
1.Baotou Medical College Center Clinical Medical College, Baotou 014040; 2.Cardiovascular Department of Baotou Central Hospital, Baotou? 014040, China
关键词:
高迁移率族蛋白1 AC16细胞自噬心肌纤维化
Keywords:
High mobility group protein AC16 cells Autophagy Myocardial fibrosis
分类号:
-
DOI:
10.3969/j.issn.1673-6583.2024.02.012
文献标识码:
-
摘要:
目的:探究高迁移率族蛋白1(HMGB1)通过调控自噬活性对心肌纤维化的影响及作用机制。方法:将人心肌细胞AC16培养于DMEM培养基中,用不同浓度的HMGB1(0、4、20、100μg/L)干预AC16细胞6h,免疫荧光染色检测心脏成纤维细胞活化的标志性蛋白α平滑肌肌动蛋白(α-SMA)的表达水平,Westernblot法检测心肌自噬相关蛋白哺乳动物雷帕霉素靶蛋白(mTOR)、磷酸化mTOR(p-mTOR)、微管相关蛋白1轻链3(LC3)、磷酸肌醇-3-激酶3(PIK3C3)、可溶性及不可溶性P62、α-
Abstract:
Objective: To explore the effect of high mobility group box protein 1 (HMGB1) on myocardial fibrosis by regulating autophagy activity of human cardiomyocytes (AC16) and its possible mechanism.? Methods:AC16 cells were cultured in DMEM medium and treated w

参考文献/References

[1] Lu C, Yang Y, Zhu Y, et al. An intervention target for myocardial fibrosis: autophagy[J]. Biomed Res Int, 2018, 2018:6215916.
[2] 洪子, 杨巍. 心肌纤维化发病机制及治疗的研究进展[J]. 临床与病理杂志, 2022, 42(1):220-225.
[3] Levine B, Kroemer G. Autophagy in the pathogenesis of disease[J]. Cell, 2008, 132(1):27-42.
[4] Pellegrini L, Foglio E, Pontemezzo E, et al. HMGB1 and repair:focus on the heart[J]. Pharmacol Ther, 2019, 196:160-182.
[5] Lotze MT, Tracey KJ. High-mobility group box 1 protein (HMGB1): nuclear weapon in the immune arsenal[J]. Nat Rev Immunol, 2005, 5(4):331-342.
[6] Park S, Ranjbarvaziri S, Zhao P, et al. Cardiac fibrosis is associated with decreased circulating levels of full-length CILP in heart failure[J]. JACC Basic Transl Sci, 2020, 5(5):432-443.
[7] Fan D, Takawale A, Lee J, et al. Cardiac fibroblasts, fibrosis and extracellular matrix remodeling in heart disease[J]. Fibrogenesis Tissue Repair, 2012, 5(1):15.
[8] Travers JG, Kamal FA, Robbins J, et al. Cardiac fibrosis: the fibroblast awakens[J]. Circ Res, 2016, 118(6):1021-1040.
[9] Parim B, Sathibabu Uddandrao VV, Saravanan G. Diabetic cardiomyopathy: molecular mechanisms, detrimental effects of conventional treatment, and beneficial effects of natural therapy[J]. Heart Fail Rev, 2019, 24(2):279-299.
[10] Yun W, Qian L, Yuan R, et al. Periplocymarin protects against myocardial fibrosis induced by β-adrenergic activation in mice[J]. Biomed Pharmacother, 2021, 139:111562.
[11] Li Y, Liu M, Song X, et al. Exogenous hydrogen sulfide ameliorates diabetic myocardial fibrosis by inhibiting cell aging through SIRT6/AMPK autophagy[J]. Front Pharmacol, 2020, 11:1150.
[12] 林晓欣, 王振华. miR-29a/HMGB1信号通路在高糖高脂诱导的心肌细胞纤维化中的作用[J]. 中国临床药理学与治疗学, 2020, 25(11):1223-1232.
[13] 张妍, 田立群, 冯莹, 等. 抑制HMGB1对心肌梗死大鼠模型心肌纤维化的影响及机制研究[J]. 中国免疫学杂志, 2021, 37(8):927-930.
[14] Vicentino ARR, Carneiro VC, Allonso D, et al. Emerging role of HMGB1 in the pathogenesis of schistosomiasis liver fibrosis[J]. Front Immunol, 2018, 9:1979.
[15] Wu RN, Yu TY, Zhou JC, et al. Targeting HMGB1 ameliorates cardiac fibrosis through restoring TLR2-mediated autophagy suppression in myocardial fibroblasts[J]. Int J Cardiol, 2018, 267:156-162.
[16] Ackermann MA. Links between mTOR and the immunoproteasome:therapeutic targets for cardiac hypertrophy?[J]. J Mol Cell Cardiol, 2015, 89(Pt B):113-115.
[17] Yan L, Vatner DE, Kim SJ, et al. Autophagy in chronically ischemic myocardium[J]. Proc Natl Acad Sci U S A, 2005, 102(39):13807-13812.
[18] Kheloufi M, Rautou PE, Boulanger CM. Autophagy in the cardiovascular system[J]. Med Sci (Paris), 2017, 33(3):283-289.
[19] Pankiv S, Clausen TH, Lamark T, et al. p62/SQSTM1 binds directly to Atg8/LC3 to facilitate degradation of ubiquitinated protein aggregates by autophagy[J]. J Biol Chem, 2007, 282(33):24131-24145.
[20] Mathew R, Karp CM, Beaudoin B, et al. Autophagy suppresses tumorigenesis through elimination of p62[J]. Cell, 2009, 137(6):1062-1075.
[21] Tang D, Kang R, Zeh HJ, et al. High-mobility group box 1, oxidative stress, and disease[J]. Antioxid Redox Signal, 2011, 14(7):1315-1335.
[22] Wu CZ, Zheng JJ, Bai YH, et al. HMGB1/RAGE axis mediates the apoptosis, invasion, autophagy, and angiogenesis of the renal cell carcinoma[J]. Onco Targets Ther, 2018, 11:4501-4510.
[23] Du Y, Liu G, Zhao L, et al. Protective effect of miR-204 on doxorubicin-induced cardiomyocyte injury via HMGB1[J]. Oxid Med Cell Longev, 2020, 2020:8819771.
[24] Hu X, Zhang K, Chen Z, et al. The HMGB1-IL-17A axis contributes to hypoxia/reoxygenation injury via regulation of cardiomyocyte apoptosis and autophagy[J]. Mol Med Rep, 2018, 17(1):336-341.

备注/Memo

备注/Memo:
基金项目:内蒙古医科大学科技百万工程联合项目[YKD2020KJBW(LH)065]
通信作者:乌日娜, E-mail:46505898@qq.com
更新日期/Last Update: 2024-03-25