Jove
Visualize
联系我们
JoVE
x logofacebook logolinkedin logoyoutube logo
关于 JoVE
概览领导团队博客JoVE 帮助中心
作者
出版流程编辑委员会范围与政策同行评审常见问题投稿
图书馆员
用户评价订阅访问资源图书馆顾问委员会常见问题
研究
JoVE JournalMethods CollectionsJoVE Encyclopedia of Experiments存档
教育
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab Manual教师资源中心教师网站
使用条款与条件
隐私政策
政策

相关概念视频

Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

488
Positive inotropic agents are commonly used as the first line of treatment for heart failure. One such agent is digoxin, derived from the genus Digitalis, which has been known for centuries but effectively utilized since 1785. However, these cardiac glycosides can have potentially toxic effects due to their mechanism of action, which involves inhibiting Na+/K+-ATPase and increasing contractility. Digoxin is absorbed orally and distributed in various tissues, including the CNS. It has a long...
488
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

360
The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
360
Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers01:22

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

1.2K
Class I antiarrhythmic drugs are used to treat various types of arrhythmias or irregular heart rhythms. These drugs block the sodium (Na+) channels in the cardiac cells, thereby affecting the movement of electrical impulses across the heart. Class I antiarrhythmic drugs are divided into three subgroups: Class IA, Class IB, and Class IC, each with distinct mechanisms of action and effects on the heart.
Class 1A Antiarrhythmic Drugs: These drugs work by moderately blocking sodium channels,...
1.2K
Antianginal Drugs: Calcium Channel Blockers and Ranolazine01:25

Antianginal Drugs: Calcium Channel Blockers and Ranolazine

433
Angina pectoris, a primary symptom of ischemic heart disease, requires careful pharmacological interventions. In this context, calcium channel blockers (CCBs) and ranolazine have emerged as crucial pharmacotherapeutic agents, providing deep insights into the complexities of angina management.
CCBs, a diverse class that includes dihydropyridines (nifedipine) and diphenylalkylamines (verapamil and diltiazem), exert their effect by blocking calcium channels in cardiac and smooth muscle cells. This...
433
Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers01:12

Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers

879
Class III antiarrhythmic drugs are a group of medications that can prolong action potentials in the heart. They achieve this by blocking potassium channels or enhancing inward currents from sodium channels. However, these drugs have a unique property of "reverse use-dependence," which is most pronounced at slower heart rates and can lead to torsades de pointes—a specific type of arrhythmia. However, it is essential to note that excessive QT interval prolongation—a measure of...
879
Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers01:24

Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers

695
Adrenergic stimulation generally impacts cardiac rate and rhythm. Specifically, stimulation of the β-adrenoceptors triggers an increase in intracellular calcium ion influx and pacemaker currents, which may cause arrhythmias. Catecholamines like adrenaline also demonstrate β2-adrenoceptor-mediated hypokalemia, impacting cardiac action potential and disrupting the normal cardiac rhythm. Class II antiarrhythmic drugs are β-adrenoceptor antagonists or β-blockers, which...
695

您也可能阅读

相关文章

通过共同作者、期刊和引用图与本文相关的文章。

排序
Same author

Synthesis of Hierarchical ZSM-5 Zeolite Mesocrystals with Controllable Macropores toward Enhanced Catalytic Performance.

Inorganic chemistry·2026
Same author

Spatially distributed carbon quantum dots in TiO<sub>2</sub> for photothermal-assisted hydrogen production from seawater.

Chemical communications (Cambridge, England)·2026
Same author

Surface SO<sub>x</sub> Species Stabilized Metal-Oxygen Bonds in PtNi Nanoalloy for Highly Efficient and Durable Seawater Hydrogen Production.

Advanced materials (Deerfield Beach, Fla.)·2026
Same author

Continuous π-Conjugation in β-Ketoenamine Covalent Organic Frameworks Boosts Charge Transfer for Selective Photocatalysis.

ACS applied materials & interfaces·2026
Same author

Physiological Responses of Apple to Nitrogen Fertilization Regimes: Roles of Calcium Metabolism in Fruit Quality and Bitter Pit Development.

Plants (Basel, Switzerland)·2026
Same author

Vericiguat protects against doxorubicin-induced myocardial injury by modulating glycolysis and histone lactylation through RELB regulation.

Biochemical pharmacology·2026

相关实验视频

Updated: May 23, 2025

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
05:14

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo

Published on: May 16, 2020

4.4K

AMD1,一个心脏毒性目标的maduramicinicin.

Zi-Feng Xie1,2, Han-Meng Liu2, Jia-Fan Zhao2

  • 1Department of Anesthesiology, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning, 121000, China.

BMC pharmacology & toxicology
|March 12, 2025
PubMed
概括

马杜拉米辛通过增加AMD1基因表达而导致心脏损伤. 减少AMD1可以缓解maduramicinicin的作用.

关键词:
在AMD1 AMD1中.马杜拉米西尼是什么意思 马杜拉米西尼是什么意思微观环境是一个微观环境.

更多相关视频

A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish
08:09

A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish

Published on: June 7, 2018

9.7K
Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy
07:40

Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy

Published on: May 26, 2023

1.0K

相关实验视频

Last Updated: May 23, 2025

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
05:14

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo

Published on: May 16, 2020

4.4K
A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish
08:09

A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish

Published on: June 7, 2018

9.7K
Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy
07:40

Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy

Published on: May 26, 2023

1.0K

科学领域:

  • 心血管毒理学心血管毒理学
  • 分子生物学分子生物学
  • 基因表达分析 基因表达分析

背景情况:

  • 马杜拉米辛 (Mad) 是一种具有已知毒性的离子体抗生素.
  • 马杜拉米辛诱导心脏毒性的特定机制尚未完全理解.
  • 在马杜拉米辛心脏毒性中阿尔金酸酶 (AMD1) 的作用需要研究.

研究的目的:

  • 在马杜拉米辛治疗的老鼠中研究AMD1的心脏毒性功能.
  • 阐明马杜拉米辛诱导的心肌损伤背后的分子机制.
  • 评估针对AMD1.1的治疗潜力.

主要方法:

  • 在体内研究中,使用Sprague-Dawley大鼠接受Maduramicin治疗.
  • 在体外实验中使用细胞模型来评估细胞亡和基因表达.
  • 使用siRNA对AMD1进行基因淘汰,以评估其功能作用.
  • 生物信息分析包括基因本体学 (GO),KEGG通路,蛋白与蛋白相互作用 (PPI),免疫透和分子对接.

主要成果:

  • 马杜拉米辛在体内和体外诱导了显著的心肌毒性作用,与AMD1水平升高有关.
  • 击败AMD1缓解了马杜拉米辛诱导的心脏毒性.
  • 关键的病理生理变化包括改变的亡,增殖和炎症,涉及IL1A,IL1B,PTGS2,VEGFA,VEGFC和HBEFG等基因.
  • 在心肌微环境中,AMD1 knockdown调节免疫细胞透.

结论:

  • 马杜拉米辛主要通过上调AMD1基因来产生心脏毒性作用.
  • AMD1在maduramicin心脏毒性中起着至关重要的作用,影响心肌细胞及其微环境.
  • 向AMD1可能提供一种治疗策略,以减轻马杜拉米辛引起的心脏损伤.