• 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

压力超负荷所致心脏氧化损伤的分子调控及治疗应用新进展

New Progress in the Molecular Regulations and Therapeutic Applications in Cardiac Oxidative Damage Caused by Pressure Overload.

作者信息

Shi Xiaomeng, Dorsey Arin, Qiu Hongyu

机构信息

Center for Molecular and Translational Medicine, Institute of Biomedical Science, Georgia State University, Atlanta, GA 30303, USA.

出版信息

Antioxidants (Basel). 2022 Apr 29;11(5):877. doi: 10.3390/antiox11050877.

DOI:10.3390/antiox11050877
PMID:35624741
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9137593/
Abstract

Chronic pressure overload is a key risk factor for mortality due to its subsequent development of heart failure, in which the underlying molecular mechanisms remain vastly undetermined. In this review, we updated the latest advancements for investigating the role and relevant mechanisms of oxidative stress involved in the pathogenesis of pressure-overload-induced cardiomyopathy and cardiac dysfunction, focusing on significant biological sources of reactive oxygen species (free radical) production, antioxidant defenses, and their association with the cardiac metabolic remodeling in the stressed heart. We also summarize the newly developed preclinical therapeutic approaches in animal models for pressure-overload-induced myocardial damage. This review aims to enhance the current understanding of the mechanisms of chronic hypertensive heart failure and potentially improve the development of better therapeutic strategies for the associated diseases.

摘要

慢性压力超负荷是导致心力衰竭死亡的关键风险因素,但其潜在的分子机制仍未明确。在本综述中,我们更新了关于氧化应激在压力超负荷诱导的心肌病和心脏功能障碍发病机制中的作用及相关机制的最新研究进展,重点关注活性氧(自由基)产生的重要生物学来源、抗氧化防御及其与应激心脏中心脏代谢重塑的关联。我们还总结了在动物模型中针对压力超负荷诱导的心肌损伤新开发的临床前治疗方法。本综述旨在加深对慢性高血压性心力衰竭机制的当前理解,并可能改善相关疾病更好治疗策略的开发。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8276/9137593/d5404ad52363/antioxidants-11-00877-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8276/9137593/d953b5ad5000/antioxidants-11-00877-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8276/9137593/d5404ad52363/antioxidants-11-00877-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8276/9137593/d953b5ad5000/antioxidants-11-00877-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8276/9137593/d5404ad52363/antioxidants-11-00877-g002.jpg

相似文献

1
New Progress in the Molecular Regulations and Therapeutic Applications in Cardiac Oxidative Damage Caused by Pressure Overload.压力超负荷所致心脏氧化损伤的分子调控及治疗应用新进展
Antioxidants (Basel). 2022 Apr 29;11(5):877. doi: 10.3390/antiox11050877.
2
EUK-8, a superoxide dismutase and catalase mimetic, reduces cardiac oxidative stress and ameliorates pressure overload-induced heart failure in the harlequin mouse mutant.EUK-8是一种超氧化物歧化酶和过氧化氢酶模拟物,可减轻心脏氧化应激,并改善丑角小鼠突变体中压力超负荷诱导的心力衰竭。
J Am Coll Cardiol. 2006 Aug 15;48(4):824-32. doi: 10.1016/j.jacc.2006.02.075. Epub 2006 Jul 25.
3
Gene expression profiles, potential targets and treatments of cardiac remodeling.心脏重塑的基因表达谱、潜在靶点及治疗方法
Mol Cell Biochem. 2025 Mar;480(3):1555-1567. doi: 10.1007/s11010-024-05126-6. Epub 2024 Oct 5.
4
Deubiquitinating enzyme CYLD mediates pressure overload-induced cardiac maladaptive remodeling and dysfunction via downregulating Nrf2.去泛素化酶 CYLD 通过下调 Nrf2 介导压力超负荷诱导的心脏适应性重构和功能障碍。
J Mol Cell Cardiol. 2015 Jul;84:143-53. doi: 10.1016/j.yjmcc.2015.04.012. Epub 2015 Apr 30.
5
Females Are Protected From Iron-Overload Cardiomyopathy Independent of Iron Metabolism: Key Role of Oxidative Stress.女性可免受铁过载心肌病的影响,与铁代谢无关:氧化应激的关键作用。
J Am Heart Assoc. 2017 Jan 23;6(1):e003456. doi: 10.1161/JAHA.116.003456.
6
Diabetic cardiomyopathy: mechanisms and new treatment strategies targeting antioxidant signaling pathways.糖尿病心肌病:抗氧化信号通路为靶点的发病机制和新治疗策略。
Pharmacol Ther. 2014 Jun;142(3):375-415. doi: 10.1016/j.pharmthera.2014.01.003. Epub 2014 Jan 22.
7
Short-Term Caloric Restriction Suppresses Cardiac Oxidative Stress and Hypertrophy Caused by Chronic Pressure Overload.短期热量限制可抑制慢性压力超负荷引起的心脏氧化应激和肥大。
J Card Fail. 2015 Aug;21(8):656-66. doi: 10.1016/j.cardfail.2015.04.016. Epub 2015 May 14.
8
Ablation of cardiac TIGAR preserves myocardial energetics and cardiac function in the pressure overload heart failure model.在压力超负荷心力衰竭模型中,消融心脏中的TIGAR可维持心肌能量代谢及心脏功能。
Am J Physiol Heart Circ Physiol. 2019 Jun 1;316(6):H1366-H1377. doi: 10.1152/ajpheart.00395.2018. Epub 2019 Mar 22.
9
Preconditioning with Short-term Dietary Restriction Attenuates Cardiac Oxidative Stress and Hypertrophy Induced by Chronic Pressure Overload.短期饮食限制预处理可减轻慢性压力超负荷引起的心脏氧化应激和肥大。
Nutrients. 2021 Feb 26;13(3):737. doi: 10.3390/nu13030737.
10
Involvement of cytosolic and mitochondrial iron in iron overload cardiomyopathy: an update.细胞溶质和线粒体铁在铁过载性心肌病中的作用:最新进展。
Heart Fail Rev. 2018 Sep;23(5):801-816. doi: 10.1007/s10741-018-9700-5.

引用本文的文献

1
Advances in the study of nicotinamide adenine dinucleotide phosphate oxidase in myocardial remodeling.心肌重塑中烟酰胺腺嘌呤二核苷酸磷酸氧化酶的研究进展
Front Cardiovasc Med. 2022 Nov 3;9:1000578. doi: 10.3389/fcvm.2022.1000578. eCollection 2022.

本文引用的文献

1
Mitochondria in Pathological Cardiac Hypertrophy Research and Therapy.病理性心肌肥大研究与治疗中的线粒体
Front Cardiovasc Med. 2022 Jan 18;8:822969. doi: 10.3389/fcvm.2021.822969. eCollection 2021.
2
Knockout of AMPKα2 Blocked the Protection of Sestrin2 Overexpression Against Cardiac Hypertrophy Induced by Pressure Overload.敲除AMPKα2可阻断Sestrin2过表达对压力超负荷诱导的心肌肥大的保护作用。
Front Pharmacol. 2021 Nov 17;12:716884. doi: 10.3389/fphar.2021.716884. eCollection 2021.
3
Beta3-Adrenergic Receptor Activation Alleviates Cardiac Dysfunction in Cardiac Hypertrophy by Regulating Oxidative Stress.
β3-肾上腺素能受体激活通过调节氧化应激减轻心脏肥厚中的心脏功能障碍。
Oxid Med Cell Longev. 2021 Oct 4;2021:3417242. doi: 10.1155/2021/3417242. eCollection 2021.
4
Joint Cardioprotective Effect of Vitamin C and Other Antioxidants against Reperfusion Injury in Patients with Acute Myocardial Infarction Undergoing Percutaneous Coronary Intervention.维生素 C 与其他抗氧化剂对行经皮冠状动脉介入治疗的急性心肌梗死患者再灌注损伤的联合心脏保护作用。
Molecules. 2021 Sep 21;26(18):5702. doi: 10.3390/molecules26185702.
5
Enhanced oxidative stress mediates pathological autophagy and necroptosis in cardiac myocytes in pressure overload induced heart failure in rats.增强的氧化应激介导大鼠压力超负荷诱导的心力衰竭中心肌细胞的病理性自噬和坏死性凋亡。
Clin Exp Pharmacol Physiol. 2022 Jan;49(1):60-69. doi: 10.1111/1440-1681.13583. Epub 2021 Sep 20.
6
Left Ventricular SGLT1 Protein Expression Correlates with the Extent of Myocardial Nitro-Oxidative Stress in Rats with Pressure and Volume Overload-Induced Heart Failure.左心室SGLT1蛋白表达与压力和容量超负荷诱导的心力衰竭大鼠心肌硝基氧化应激程度相关。
Antioxidants (Basel). 2021 Jul 26;10(8):1190. doi: 10.3390/antiox10081190.
7
NLRP3 inflammasome activation contributes to the pathogenesis of cardiocytes aging.NLRP3 炎性小体的激活有助于心肌细胞衰老的发病机制。
Aging (Albany NY). 2021 Aug 25;13(16):20534-20551. doi: 10.18632/aging.203435.
8
Cardioprotective effects of early intervention with sacubitril/valsartan on pressure overloaded rat hearts.早期应用沙库巴曲缬沙坦对压力超负荷大鼠心脏的心脏保护作用。
Sci Rep. 2021 Aug 16;11(1):16542. doi: 10.1038/s41598-021-95988-3.
9
Multiple roles of cardiac macrophages in heart homeostasis and failure.心脏巨噬细胞在心脏稳态和衰竭中的多重作用。
Heart Fail Rev. 2022 Jul;27(4):1413-1430. doi: 10.1007/s10741-021-10156-z. Epub 2021 Aug 13.
10
Qindan Capsule Attenuates Myocardial Hypertrophy and Fibrosis in Pressure Overload-Induced Mice Involving mTOR and TGF-1/Smad Signaling Pathway Inhibition.芩丹胶囊通过抑制mTOR和TGF-1/Smad信号通路减轻压力超负荷诱导小鼠的心肌肥厚和纤维化。
Evid Based Complement Alternat Med. 2021 Apr 28;2021:5577875. doi: 10.1155/2021/5577875. eCollection 2021.