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Related Concept Videos

Cardiomyopathy II: Dilated Cardiomyopathy01:30

Cardiomyopathy II: Dilated Cardiomyopathy

Dilated cardiomyopathy, or DCM, is a progressive myocardial disorder characterized by ventricular chamber dilation and contractile dysfunction.EtiologyVarious factors can cause DCM, including hypertension and heavy alcohol intake, which contribute to the weakening and enlargement of the heart muscle. Viral infections, such as Coxsackievirus B, adenoviruses, and influenza, can lead to DCM by causing inflammation and damage to heart tissue. Certain chemotherapeutic agents, including daunorubicin,...
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

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...
Cardiomyopathy IV: Restrictive Cardiomyopathy01:29

Cardiomyopathy IV: Restrictive Cardiomyopathy

Restrictive cardiomyopathy (RCM) is a rare heart muscle disease characterized by impaired ventricular filling due to stiffened ventricular walls, leading to significant diastolic dysfunction.EtiologyRestrictive cardiomyopathy can arise from both inherited and acquired diseases, many of which are systemic. It is categorized into four main types: infiltrative, storage, non-infiltrative, and endomyocardial diseases.Infiltrative diseases, such as amyloidosis, lead to RCM by depositing amyloid...
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

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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Cardiomyopathy V: Interprofessional Care

Managing cardiomyopathy involves addressing underlying or precipitating causes, treating heart failure with medications, and implementing dietary changes and a balanced exercise and rest regimen.Lifestyle ModificationsCardiomyopathy patients should adopt a low-sodium diet to reduce fluid retention and manage heart failure. A personalized exercise and rest plan helps maintain physical fitness without overstraining the heart. Avoiding alcohol and tobacco is essential to prevent further damage to...

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Updated: May 12, 2026

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
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Published on: May 16, 2020

Anthracycline cardiotoxicity.

Pierantonio Menna1, Emanuela Salvatorelli, Luca Gianni

  • 1University Campus Bio-Medico of Rome, CIR and Drug Sciences, Via Alvaro del Portillo 21, 00128, Rome, Italy.

Topics in Current Chemistry
|April 23, 2013
PubMed
Summary
This summary is machine-generated.

Doxorubicin cardiotoxicity is linked to its plasma concentration and heart diffusion, involving specific reduction pathways. Strategies like slow infusion and antioxidants may reduce cardiac damage from anthracyclines.

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Last Updated: May 12, 2026

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04:48

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Published on: January 7, 2015

Area of Science:

  • Pharmacology
  • Cardiology
  • Oncology

Background:

  • Doxorubicin and related anthracyclines are vital anticancer drugs.
  • Their clinical utility is significantly limited by dose-dependent cardiotoxicity.
  • Understanding the mechanisms of anthracycline cardiotoxicity is crucial for developing safer treatments.

Purpose of the Study:

  • To review the correlation between doxorubicin's peak plasma concentration, cardiac diffusion, and cardiotoxicity.
  • To elucidate the role of reductive bioactivation and oxidative inactivation in anthracycline-induced cardiotoxicity.
  • To discuss mechanism-based cardioprotective strategies and novel anthracycline analogs.

Main Methods:

  • Review of preclinical modeling and clinical studies on anthracycline cardiotoxicity.
  • Analysis of metabolic pathways including one-electron quinone reduction and two-electron side chain carbonyl reduction.
  • Evaluation of oxidative inactivation via one-electron hydroquinone oxidation.
  • Assessment of cardioprotective strategies such as altered administration and drug formulation.

Main Results:

  • Anthracycline cardiotoxicity is associated with one-electron quinone reduction and two-electron side chain carbonyl reduction, involving iron and free radical reactions.
  • One-electron hydroquinone oxidation acts as a detoxification pathway.
  • Strategies like slow infusion, liposomal encapsulation, antioxidants, and iron chelators show promise in cardioprotection.
  • Eliminating the side chain carbonyl group reduction significantly enhances cardioprotection.

Conclusions:

  • Doxorubicin cardiotoxicity is mechanistically linked to specific metabolic activation pathways.
  • Novel cardioprotective strategies, including modified drug administration and chemical structure, can mitigate cardiac damage.
  • Anthracyclines lacking the carbonyl group or resistant to its reduction may offer improved safety profiles, especially with newer combination therapies.