• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法，用中文像聊天一样搜索，搜遍4000万医学文献。AI智能推荐，让科研检索更轻松。

立即免费搜索

文件翻译

保留排版，准确专业，支持PDF/Word/PPT等文件格式，支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述，25分钟生成高质量综述，智能提取关键信息，辅助科研写作。

立即免费体验

miRNA-145 通过 Akt3/mTOR 信号通路抑制心肌梗死后的细胞凋亡，从而抑制心肌梗死后的细胞凋亡，在体外和体内。

miRNA‑145 inhibits myocardial infarction‑induced apoptosis through autophagy via Akt3/mTOR signaling pathway in vitro and in vivo.

机构信息

Department of Cardiology, Cangzhou Central Hospital, Hebei Medical University, Cangzhou, Hebei 061000, P.R. China.

出版信息

Int J Mol Med. 2018 Sep;42(3):1537-1547. doi: 10.3892/ijmm.2018.3748. Epub 2018 Jun 28.

DOI:10.3892/ijmm.2018.3748
PMID:29956747
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6089768/
Abstract

The present study investigated the effects of micro (mi)RNA‑145 on acute myocardial infarction (AMI) and the potential underlying mechanism. A total of 6 AMI and 6 normal rat tissues were investigated for the present study. It was demonstrated that miRNA‑145 expression was downregulated in the AMI rat model, compared with the control group. Downregulation of miRNA‑145 increased cardiac cell apoptosis, suppressed phosphorylated (p)‑RAC‑γ serine/threonine‑protein kinase (Akt3) and p‑mechanistic target of rapamycin (mTOR) protein expression levels and suppressed autophagy in an in vitro model of AMI. However, overexpression of miRNA‑145 decreased cardiac cell apoptosis, induced p‑Akt3 and p‑mTOR protein expression and promoted autophagy in the in vitro model of AMI. The inhibition of Akt3 (GSK2110183, 1 nM) decreased the effect of the miRNA‑145 upregulation on cell apoptosis in the in vitro model of AMI. Chloroquine diphosphate (5 µM) inhibited the regulatory effect of miRNA‑145 upregulation on autophagy to adjust cell apoptosis, in the in vitro model of AMI. The results of the present study demonstrate that miRNA‑145 inhibits myocardial infarction‑induced apoptosis via autophagy associated with the Akt3/mTOR signaling pathway in vivo and in vitro.

摘要

本研究探讨了 micro(mi)RNA-145 对急性心肌梗死(AMI)的影响及其潜在的作用机制。本研究共检测了 6 例 AMI 大鼠组织和 6 例正常大鼠组织。结果表明，与对照组相比，AMI 大鼠模型中 miRNA-145 的表达下调。miRNA-145 下调增加了心肌细胞凋亡，抑制了磷酸化(RAC-γ 丝氨酸/苏氨酸蛋白激酶(Akt3)和磷酸化(mTOR)蛋白表达水平，并抑制了 AMI 体外模型中的自噬。然而，miRNA-145 的过表达降低了心肌细胞凋亡，诱导了 p-Akt3 和 p-mTOR 蛋白表达，并促进了 AMI 体外模型中的自噬。Akt3(GSK2110183，1 nM)的抑制作用减弱了 miRNA-145 过表达对 AMI 体外模型中细胞凋亡的影响。氯喹二磷酸盐(5 µM)抑制了 miRNA-145 过表达对自噬的调节作用，从而调节细胞凋亡，在 AMI 的体外模型中。本研究结果表明，miRNA-145 通过 Akt3/mTOR 信号通路在体内和体外抑制心肌梗死后诱导的细胞凋亡和自噬。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7618/6089768/6511bcc5cd31/IJMM-42-03-1537-g10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7618/6089768/d61333309435/IJMM-42-03-1537-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7618/6089768/3831b6ab1f4a/IJMM-42-03-1537-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7618/6089768/9e1e6d251c2c/IJMM-42-03-1537-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7618/6089768/e47f9c7f8f4f/IJMM-42-03-1537-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7618/6089768/482f9cffaa69/IJMM-42-03-1537-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7618/6089768/14d0ff632bee/IJMM-42-03-1537-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7618/6089768/1c6fec46e1cd/IJMM-42-03-1537-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7618/6089768/5b26aa07fd10/IJMM-42-03-1537-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7618/6089768/a6f89a78a866/IJMM-42-03-1537-g08.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7618/6089768/0c77d8151671/IJMM-42-03-1537-g09.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7618/6089768/6511bcc5cd31/IJMM-42-03-1537-g10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7618/6089768/d61333309435/IJMM-42-03-1537-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7618/6089768/3831b6ab1f4a/IJMM-42-03-1537-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7618/6089768/9e1e6d251c2c/IJMM-42-03-1537-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7618/6089768/e47f9c7f8f4f/IJMM-42-03-1537-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7618/6089768/482f9cffaa69/IJMM-42-03-1537-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7618/6089768/14d0ff632bee/IJMM-42-03-1537-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7618/6089768/1c6fec46e1cd/IJMM-42-03-1537-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7618/6089768/5b26aa07fd10/IJMM-42-03-1537-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7618/6089768/a6f89a78a866/IJMM-42-03-1537-g08.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7618/6089768/0c77d8151671/IJMM-42-03-1537-g09.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7618/6089768/6511bcc5cd31/IJMM-42-03-1537-g10.jpg

相似文献

1
miRNA‑145 inhibits myocardial infarction‑induced apoptosis through autophagy via Akt3/mTOR signaling pathway in vitro and in vivo.miRNA-145 通过 Akt3/mTOR 信号通路抑制心肌梗死后的细胞凋亡，从而抑制心肌梗死后的细胞凋亡，在体外和体内。
Int J Mol Med. 2018 Sep;42(3):1537-1547. doi: 10.3892/ijmm.2018.3748. Epub 2018 Jun 28.
2
MicroRNA-223 protects neonatal rat cardiomyocytes and H9c2 cells from hypoxia-induced apoptosis and excessive autophagy via the Akt/mTOR pathway by targeting PARP-1.miR-223 通过靶向 PARP-1 保护新生大鼠心肌细胞和 H9c2 细胞免于缺氧诱导的凋亡和过度自噬，通过 Akt/mTOR 通路。
J Mol Cell Cardiol. 2018 May;118:133-146. doi: 10.1016/j.yjmcc.2018.03.018. Epub 2018 Mar 31.
3
Autophagy participates in the protection role of 1,25-dihydroxyvitamin D3 in acute myocardial infarction via PI3K/AKT/mTOR pathway.自噬通过 PI3K/AKT/mTOR 通路参与 1,25-二羟维生素 D3 在急性心肌梗死中的保护作用。
Cell Biol Int. 2021 Feb;45(2):394-403. doi: 10.1002/cbin.11495. Epub 2020 Nov 25.
4
Tongxinluo exerts protective effects via anti-apoptotic and pro-autophagic mechanisms by activating AMPK pathway in infarcted rat hearts.通心络通过激活梗死大鼠心脏中的AMPK途径，经由抗凋亡和促自噬机制发挥保护作用。
Exp Physiol. 2017 Apr 1;102(4):422-435. doi: 10.1113/EP086192. Epub 2017 Mar 14.
5
MicroRNA‑494 suppresses hypoxia/reoxygenation‑induced cardiomyocyte apoptosis and autophagy via the PI3K/AKT/mTOR signaling pathway by targeting SIRT1.MicroRNA-494 通过靶向 SIRT1 抑制低氧/复氧诱导的心肌细胞凋亡和自噬通过 PI3K/AKT/mTOR 信号通路。
Mol Med Rep. 2020 Dec;22(6):5231-5242. doi: 10.3892/mmr.2020.11636. Epub 2020 Oct 26.
6
CircCDR1as upregulates autophagy under hypoxia to promote tumor cell survival via AKT/ERK/mTOR signaling pathways in oral squamous cell carcinomas.环状 RNA CDR1as 在低氧环境下上调自噬，通过 AKT/ERK/mTOR 信号通路促进口腔鳞状细胞癌肿瘤细胞存活。
Cell Death Dis. 2019 Oct 3;10(10):745. doi: 10.1038/s41419-019-1971-9.
7
Knockdown of insulin-like growth factor 1 exerts a protective effect on hypoxic injury of aged BM-MSCs: role of autophagy.敲低胰岛素样生长因子 1 对缺氧损伤的老年 BM-MSCs 发挥保护作用：自噬的作用。
Stem Cell Res Ther. 2018 Oct 25;9(1):284. doi: 10.1186/s13287-018-1028-5.
8
Trimetazidine protects against myocardial ischemia/reperfusion injury by inhibiting excessive autophagy.曲美他嗪通过抑制过度自噬来保护心肌免受缺血/再灌注损伤。
J Mol Med (Berl). 2018 Aug;96(8):791-806. doi: 10.1007/s00109-018-1664-3. Epub 2018 Jun 29.
9
Cannabinoid receptor 2 deletion deteriorates myocardial infarction through the down-regulation of AMPK-mTOR-p70S6K signaling-mediated autophagy.大麻素受体 2 缺失通过下调 AMPK-mTOR-p70S6K 信号通路介导的自噬来加重心肌梗死。
Biosci Rep. 2019 Apr 26;39(4). doi: 10.1042/BSR20180650. Print 2019 Apr 30.
10
Sevoflurane ameliorates doxorubicin-induced myocardial injury by affecting the phosphorylation states of proteins in PI3K/Akt/mTOR signaling pathway.七氟醚通过影响PI3K/Akt/mTOR信号通路中蛋白质的磷酸化状态来改善阿霉素诱导的心肌损伤。
Cardiol J. 2017;24(4):409-418. doi: 10.5603/CJ.a2017.0018. Epub 2017 Feb 15.

引用本文的文献

1
Therapeutic Relevance of Inducing Autophagy in β-Thalassemia.β-地中海贫血症中诱导自噬的治疗相关性。
Cells. 2024 May 25;13(11):918. doi: 10.3390/cells13110918.
2
Identification of co-expressed central genes and transcription factors in acute myocardial infarction and diabetic nephropathy.鉴定急性心肌梗死和糖尿病肾病中的共表达中枢基因和转录因子。
BMC Med Genomics. 2024 May 20;17(1):134. doi: 10.1186/s12920-024-01906-7.
3
The emerging roles of miRNA-mediated autophagy in ovarian cancer.微小RNA介导的自噬在卵巢癌中的新作用

本文引用的文献

1
WITHDRAWN: Cardamonin attenuates lung carcinoma and promotes autophagy via targeting p53 and regulating Mtor.撤回：小豆蔻明通过靶向p53和调节雷帕霉素靶蛋白（mTOR）来减轻肺癌并促进自噬。
Eur J Pharmacol. 2017 Jul 14. doi: 10.1016/j.ejphar.2017.07.021.
2
Circadian MicroRNAs in Cardioprotection.昼夜节律 microRNAs 在心脏保护中的作用。
Curr Pharm Des. 2017;23(25):3723-3730. doi: 10.2174/1381612823666170707165319.
3
Oestrogen Inhibits Arterial Calcification by Promoting Autophagy.雌激素通过促进自噬来抑制动脉钙化。
Cell Death Dis. 2024 May 3;15(5):314. doi: 10.1038/s41419-024-06677-8.
4
P-MSC-derived extracellular vesicles facilitate diabetic wound healing via miR-145-5p/ CDKN1A-mediated functional improvements of high glucose-induced senescent fibroblasts.源自胎盘间充质干细胞的细胞外囊泡通过miR-145-5p/CDKN1A介导的高糖诱导衰老成纤维细胞功能改善促进糖尿病伤口愈合。
Burns Trauma. 2023 Oct 18;11:tkad010. doi: 10.1093/burnst/tkad010. eCollection 2023.
5
MBNL1-AS1 Promotes Hypoxia-Induced Myocardial Infarction via the miR-132-3p/RAB14/CAMTA1 Axis.MBNL1-AS1 通过 miR-132-3p/RAB14/CAMTA1 轴促进缺氧诱导的心肌梗死。
Oxid Med Cell Longev. 2023 Feb 4;2023:3308725. doi: 10.1155/2023/3308725. eCollection 2023.
6
Exercise improves cardiac function in the aged rats with myocardial infarction.运动改善心肌梗死后老年大鼠的心脏功能。
Physiol Res. 2023 Mar 8;72(1):27-35. doi: 10.33549/physiolres.934966. Epub 2022 Dec 22.
7
Insight into the Role of the PI3K/Akt Pathway in Ischemic Injury and Post-Infarct Left Ventricular Remodeling in Normal and Diabetic Heart.解析 PI3K/Akt 通路在正常和糖尿病心脏缺血性损伤及梗死后左心室重构中的作用。
Cells. 2022 May 5;11(9):1553. doi: 10.3390/cells11091553.
8
Circular RNA Sirtuin1 represses pulmonary artery smooth muscle cell proliferation, migration and autophagy to ameliorate pulmonary hypertension via targeting microRNA-145-5p/protein kinase-B3 axis.环状RNA沉默调节蛋白1通过靶向微小RNA-145-5p/蛋白激酶B3轴抑制肺动脉平滑肌细胞增殖、迁移和自噬，从而改善肺动脉高压。
Bioengineered. 2022 Apr;13(4):8759-8771. doi: 10.1080/21655979.2022.2036302.
9
The Key Genes Underlying Pathophysiology Correlation Between the Acute Myocardial Infarction and COVID-19.急性心肌梗死与新型冠状病毒肺炎病理生理关联的关键基因
Int J Gen Med. 2022 Mar 4;15:2479-2490. doi: 10.2147/IJGM.S354885. eCollection 2022.
10
Targeting Epigenetics and Non-coding RNAs in Myocardial Infarction: From Mechanisms to Therapeutics.靶向心肌梗死中的表观遗传学和非编码RNA：从机制到治疗
Front Genet. 2021 Dec 20;12:780649. doi: 10.3389/fgene.2021.780649. eCollection 2021.
Sci Rep. 2017 Jun 14;7(1):3549. doi: 10.1038/s41598-017-03801-x.
4
MicroRNA-34a protects myocardial cells against ischemia-reperfusion injury through inhibiting autophagy via regulating TNFα expression.微小RNA-34a通过调节肿瘤坏死因子α（TNFα）的表达抑制自噬，从而保护心肌细胞免受缺血-再灌注损伤。
Biochem Cell Biol. 2018 Jun;96(3):349-354. doi: 10.1139/bcb-2016-0158. Epub 2017 May 25.
5
The mTOR Signaling Pathway in Myocardial Dysfunction in Type 2 Diabetes Mellitus.2型糖尿病心肌功能障碍中的mTOR信号通路
Curr Diab Rep. 2017 Jun;17(6):38. doi: 10.1007/s11892-017-0865-4.
6
Risk Stratification for Patients in Cardiogenic Shock After Acute Myocardial Infarction.心肌梗死后心源性休克患者的风险分层。
J Am Coll Cardiol. 2017 Apr 18;69(15):1913-1920. doi: 10.1016/j.jacc.2017.02.027.
7
MicroRNA-145 inhibits the activation of the mTOR signaling pathway to suppress the proliferation and invasion of invasive pituitary adenoma cells by targeting AKT3 in vivo and in vitro.微小RNA-145在体内和体外通过靶向AKT3抑制mTOR信号通路的激活，从而抑制侵袭性垂体腺瘤细胞的增殖和侵袭。
Onco Targets Ther. 2017 Mar 16;10:1625-1635. doi: 10.2147/OTT.S118391. eCollection 2017.
8
CORRIGENDUM: Circulating miR-122-5p/miR-133b Ratio Is a Specific Early Prognostic Biomarker in Acute Myocardial Infarction.勘误：循环miR-122-5p/miR-133b比值是急性心肌梗死的一种特异性早期预后生物标志物。
Circ J. 2017;81(4):613. doi: 10.1253/circj.CJ-66-0140.
9
Hypoxic preconditioning of human cardiosphere-derived cell sheets enhances cellular functions via activation of the PI3K/Akt/mTOR/HIF-1α pathway.人心脏球衍生细胞片的低氧预处理通过激活PI3K/Akt/mTOR/HIF-1α信号通路增强细胞功能。
Am J Transl Res. 2017 Feb 15;9(2):664-673. eCollection 2017.
10
Feasibility of Extracorporeal Shock Wave Myocardial Revascularization Therapy for Post-Acute Myocardial Infarction Patients and Refractory Angina Pectoris Patients.体外冲击波心肌血运重建治疗急性心肌梗死后患者及难治性心绞痛患者的可行性
Int Heart J. 2017 Apr 6;58(2):185-190. doi: 10.1536/ihj.16-289. Epub 2017 Mar 21.