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Related Concept Videos

Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

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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...
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Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

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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...
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Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers01:22

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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,...
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Antianginal Drugs: Calcium Channel Blockers and Ranolazine01:25

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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...
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Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers01:12

Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers

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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...
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Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers01:24

Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers

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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...
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Updated: May 23, 2025

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
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AMD1, a cardiotoxicity target for Maduramicin.

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
Summary
This summary is machine-generated.

Maduramicin causes heart damage by increasing AMD1 gene expression. Reducing AMD1 alleviates Maduramicin

Keywords:
AMD1MaduramicinMicroenvironment

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Area of Science:

  • Cardiovascular toxicology
  • Molecular biology
  • Gene expression analysis

Background:

  • Maduramicin (Mad) is an ionophore antibiotic with known toxicity.
  • The specific mechanisms of Maduramicin-induced cardiotoxicity are not fully understood.
  • The role of Argininosuccinate lyase (AMD1) in Maduramicin cardiotoxicity requires investigation.

Purpose of the Study:

  • To investigate the cardiotoxicity function of AMD1 in Maduramicin-treated rats.
  • To elucidate the molecular mechanisms underlying Maduramicin-induced myocardial damage.
  • To assess the therapeutic potential of targeting AMD1.

Main Methods:

  • In vivo studies using Sprague-Dawley rats treated with Maduramicin.
  • In vitro experiments utilizing cell models to assess apoptosis and gene expression.
  • Gene knockdown of AMD1 using siRNA to evaluate its functional role.
  • Bioinformatic analyses including Gene Ontology (GO), KEGG pathway, Protein-Protein Interaction (PPI), immune infiltration, and molecular docking.

Main Results:

  • Maduramicin induced significant myocardial toxic effects in vivo and in vitro, associated with elevated AMD1 levels.
  • Knockdown of AMD1 alleviated Maduramicin-induced cardiotoxicity.
  • Key pathophysiological changes included altered apoptosis, proliferation, and inflammation, involving genes like IL1A, IL1B, PTGS2, VEGFA, VEGFC, and HBEFG.
  • AMD1 knockdown modulated immune cell infiltration in the myocardial microenvironment.

Conclusions:

  • Maduramicin exerts cardiotoxic effects primarily by upregulating the AMD1 gene.
  • AMD1 plays a crucial role in Maduramicin cardiotoxicity, influencing myocardial cells and their microenvironment.
  • Targeting AMD1 may offer a therapeutic strategy to mitigate Maduramicin-induced heart damage.