Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Cardiomyopathy II: Dilated Cardiomyopathy

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 IV: Restrictive Cardiomyopathy

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...

Cardiomyopathy III: Hypertrophic Cardiomyopathy

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 Agents

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 I: Introduction and Classification

Cardiomyopathy I: Introduction and Classification

Cardiomyopathy, or CMP, is a group of diseases affecting the myocardial structure, impairing its ability to pump blood effectively. This condition can lead to arrhythmias, heart failure, or sudden cardiac death.Cardiomyopathies are classified into primary and secondary categories:Primary Cardiomyopathy refers to conditions involving only the heart muscle that are often idiopathic (of unknown cause) or genetic. They primarily affect the myocardium without the involvement of other systemic...

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Lycopene-rich tomato oleoresin modulates plasma adiponectin concentration and mRNA levels of adiponectin, SIRT1, and FoxO1 in adipose tissue of obese rats.

Human & experimental toxicology·2015

Same author

Lycopene supplementation reduces TNF-α via RAGE in the kidney of obese rats.

Nutrition & diabetes·2014

Same author

Oxidative stress on cardiotoxicity after treatment with single and multiple doses of doxorubicin.

Human & experimental toxicology·2013

Same author

Diastolic function is associated with quality of life and exercise capacity in stable heart failure patients with reduced ejection fraction.

Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas·2013

Same author

Nutritional intake according to injury extent in ulcerative colitis patients.

Journal of human nutrition and dietetics : the official journal of the British Dietetic Association·2013

Same author

Oxidative stress status of highly prolific sows during gestation and lactation.

Animal : an international journal of animal bioscience·2012

Search research articles

Related Experiment Video

Updated: Jun 29, 2026

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo

Published on: May 16, 2020

Anthracycline-induced cardiotoxicity.

A L A Ferreira¹, L S Matsubara, B B Matsubara

¹Department of Internal Medicine, Botucatu Medical School, UNESP- São Paulo State University, Botucatu, SP, Brasil. ferreira@fmb.unesp.br

Cardiovascular & Hematological Agents in Medicinal Chemistry

|October 16, 2008

Summary

This summary is machine-generated.

Anthracyclines are vital chemotherapy drugs, but can cause irreversible cardiotoxicity. This review evaluates oxidative stress mechanisms in doxorubicin-induced heart damage and discusses clinical management.

More Related Videos

A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish

A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish

Published on: June 7, 2018

Chemotherapy-induced Vascular Toxicity - Real-time In vivo Imaging of Vessel Impairment

Chemotherapy-induced Vascular Toxicity - Real-time In vivo Imaging of Vessel Impairment

Published on: January 7, 2015

Related Experiment Videos

Last Updated: Jun 29, 2026

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo

Published on: May 16, 2020

A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish

A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish

Published on: June 7, 2018

Chemotherapy-induced Vascular Toxicity - Real-time In vivo Imaging of Vessel Impairment

Chemotherapy-induced Vascular Toxicity - Real-time In vivo Imaging of Vessel Impairment

Published on: January 7, 2015

Area of Science:

Cardiology
Oncology
Pharmacology

Background:

Anthracyclines are essential chemotherapy agents for various human tumors.
A significant limitation to their use is the development of irreversible cardiotoxicity.
Anthracycline-induced cardiotoxicity has a poor prognosis once overt heart failure develops.

Purpose of the Study:

To critically evaluate hypotheses on oxidative stress in doxorubicin-induced cardiotoxicity.
To review strategies for preventing or attenuating anthracycline side effects.
To discuss clinical diagnosis and treatment of anthracycline cardiotoxicity.

Main Methods:

Multisided approach to review existing literature.
Critical evaluation of proposed mechanisms of cardiotoxicity.
Analysis of the role of reactive oxygen species.

Main Results:

Anthracycline-induced cardiotoxicity is a serious concern with long-term implications.
Oxidative stress mediated by reactive oxygen species is a common proposed mechanism.
The efficacy of antioxidants in preventing cardiotoxicity remains controversial due to differing acute vs. chronic toxicity mechanisms.

Conclusions:

Understanding the role of oxidative stress is crucial for managing doxorubicin cardiotoxicity.
Further research is needed to clarify the complex mechanisms of anthracycline-induced cardiotoxicity.
Effective strategies for prevention and treatment are essential to improve patient outcomes.