Related Experiment Video
Updated: Jun 28, 2025
05:14
A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
Published on: May 16, 2020
4.6K
Doxorubicin conjugates: a practical approach for its cardiotoxicity alleviation
Abed Alqader Ibrahim1, Hamdi Nsairat2, Mazen Al-Sulaibi2
1Department of Nanoscience, Joint School of Nanoscience and Nanoengineering, University of North Carolina at Greensboro, Greensboro, NC, USA.
Expert Opinion on Drug Delivery
|April 16, 2024
Summary
Doxorubicin (DOX) chemotherapy causes heart damage. DOX conjugates, linking DOX to other molecules, show promise in reducing this cardiotoxicity, improving cancer treatment safety.
Area of Science:
- Oncology
- Cardiology
- Nanomedicine
Background:
- Doxorubicin (DOX) is a vital chemotherapy drug.
- DOX causes significant cardiotoxicity, leading to heart failure.
- Current strategies aim to reduce DOX's cardiac side effects.
Purpose of the Study:
- To explore DOX conjugates as a method to mitigate DOX-induced cardiotoxicity.
- To review the mechanisms and potential of DOX conjugates in cancer therapy.
- To enhance the safety profile of Doxorubicin treatment.
Main Methods:
- Review of recent scientific literature on DOX conjugates.
- Analysis of strategies involving physical or chemical conjugation of DOX.
- Examination of conjugates with moieties, polymers, biomolecules, and nanoparticles.
Main Results:
- DOX conjugates offer a promising approach to reduce cardiotoxicity.
- Conjugation strategies modulate DOX's mechanism, uptake, and targeting.
- Nanocarrier encapsulation of DOX also improves efficacy and reduces side effects.
Conclusions:
- DOX conjugates represent a significant advancement in managing chemotherapy-induced cardiac compromise.
- This strategy enhances safety margins for Doxorubicin therapy.
- DOX conjugates hold promise for refining cancer treatment outcomes.
Related Concept Videos
01:26Heart Failure Drugs: Inotropic Agents
577
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...
577
01:26Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
422
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...
422
01:12Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers
988
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...
988
01:22Heart Failure Drugs: Diuretics
370
Heart failure and kidney perfusion are interconnected in a complex way. Reduced renal perfusion and venous congestion are two significant factors that contribute to renal dysfunction in heart failure. The kidneys, primarily responsible for fluid balance in the body, are adversely affected due to compromised cardiac output and increased venous pressure. In response to reduced renal perfusion, the kidneys activate neurohumoral mechanisms to restore balance. However, these mechanisms can be...
370
01:24Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers
741
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...
741
01:22Heart Failure Drugs: β-Blockers
337
β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation,...
337