Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

1.5K
Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...
1.5K
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

12.4K
The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
12.4K
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

5.7K
Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
5.7K
Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

545
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...
545
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

405
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...
405
Cardiovascular Drugs: Classification based on Therapeutic Indications01:18

Cardiovascular Drugs: Classification based on Therapeutic Indications

2.1K
Cardiovascular diseases, encompassing a range of conditions, can significantly affect the heart's operations and the overall circulatory system. These conditions impair the heart's ability to pump blood, leading to a deficit in oxygen supply to crucial organs. Anomalies in the heart's electrical system, known as arrhythmias, can cause heartbeats to accelerate or slow down. Usually, heart rates increase during physical activity and decrease while resting or sleeping. However,...
2.1K

You might also read

Related Articles

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

Sort by
Same author

Carbon-Confined FeCo@Pt Nanocatalysts Derived from Metal-Organic Frameworks for Pt-Economical, High-Performance, and CO-Tolerant Methanol Electrooxidation.

Langmuir : the ACS journal of surfaces and colloids·2026
Same author

Signal-amplified cell-free biosensing of antibiotics using tandem fluorescent aptamers.

Talanta·2026
Same author

Climate Change Elevates the Risk of Antibiotic Resistance in Global Surface Ocean.

Global change biology·2026
Same author

Interlayer-Driven Interfacial Stabilization in Solid Electrolytes for Lithium Batteries: Promises and Challenges.

ChemSusChem·2026
Same author

Construction and Application of a Multicolor Bactosensor for Detecting Bioavailable Antibiotic Mixtures in the Environment.

ACS synthetic biology·2026
Same author

Multicomponent Simultaneous Identification Network (MSINet): An Advanced Deep Learning Model for Boosting Multiplex SERS Detection in Untreated Real Samples.

Analytical chemistry·2026

Related Experiment Video

Updated: Jun 15, 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

4.5K

Anthracycline-induced cardiotoxicity: An overview from cellular structural perspective.

Hansheng Li1, Meilun Wang1, Yan Huang1

  • 1Department of Cardiology and Cardiovascular Research Institute, Renmin Hospital of Wuhan University, Wuhan, Hubei Province 430060, China; Hubei Key Laboratory of Cardiology, Wuhan, Hubei Province 430060, China.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|August 21, 2024
PubMed
Summary

Anthracyclines fight cancer but harm the heart. This review details anthracycline-induced cardiotoxicity mechanisms and explores new therapies targeting cellular pathways for heart protection.

Keywords:
AnthracyclineCardio-OncologyCardiotoxicityCell structureMechanisms

More Related Videos

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

A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish

Published on: June 7, 2018

9.8K
Hybrid Cell Analysis System to Assess Structural and Contractile Changes of Human iPSC-Derived Cardiomyocytes for Preclinical Cardiac Risk Evaluation
08:03

Hybrid Cell Analysis System to Assess Structural and Contractile Changes of Human iPSC-Derived Cardiomyocytes for Preclinical Cardiac Risk Evaluation

Published on: October 20, 2022

1.8K

Related Experiment Videos

Last Updated: Jun 15, 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

4.5K
A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish
08:09

A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish

Published on: June 7, 2018

9.8K
Hybrid Cell Analysis System to Assess Structural and Contractile Changes of Human iPSC-Derived Cardiomyocytes for Preclinical Cardiac Risk Evaluation
08:03

Hybrid Cell Analysis System to Assess Structural and Contractile Changes of Human iPSC-Derived Cardiomyocytes for Preclinical Cardiac Risk Evaluation

Published on: October 20, 2022

1.8K

Area of Science:

  • Cardiology
  • Oncology
  • Molecular Biology

Background:

  • Anthracyclines are vital anticancer agents with dose-limiting cardiotoxicity.
  • Anthracycline-induced cardiotoxicity (AIC) is a major cause of mortality in cancer survivors.
  • Understanding AIC mechanisms is crucial for improving cancer treatment outcomes.

Purpose of the Study:

  • To review and update the known mechanisms of AIC.
  • To focus on cellular-level effects of AIC.
  • To explore novel therapeutic strategies for AIC.

Main Methods:

  • Literature review of established and emerging AIC mechanisms.
  • Analysis of cellular pathways and organelles involved in AIC.
  • Evaluation of potential therapeutic targets for AIC.

Main Results:

  • Established mechanisms include reactive oxygen species and topoisomerase II beta inhibition, with mitochondria as a key organelle.
  • Emerging mechanisms involve ferroptosis, calcium overload, autophagy, and inflammation.
  • Diverse cellular levels contribute to the complex pathophysiology of AIC.

Conclusions:

  • AIC involves multiple, interconnected cellular mechanisms.
  • Targeting specific organelles and pathways offers promising therapeutic avenues.
  • Further research into AIC mechanisms can lead to safer, more effective cancer therapies.