Mini Review - Current Trends in Cardiology (2023) Volume 7, Issue 8

Cardio toxicity advances in pharmacogenomics and personalized medicine

Devesh Rai^*

Department of Cardiology, Sands?Constellation Heart Institute, Rochester, New York.

*Corresponding Author:

Devesh Rai
Department of Cardiology
Sands?Constellation Heart Institute
Rochester, New York.
E-mail: Deveshrai@gmail.com

Received:31-Jul-2023, Manuscript No. AACC-23-107497; Editor assigned: 02-Aug-2023,PreQC No. AACC-23-107497(PQ); Reviewed:17-Aug-2023,QC No. AACC-23-107497; Revised:22-Aug-2023, Manuscript No. AACC-23-107497 (R); Published:29-Aug-2023,DOI:10.35841/aacc-7.8.193

Citation: Rai D. Cardio toxicity advances in pharmacogenomics and personalized medicine. J Cell Biol Metab. 2023;7(8):193

Abstract

Cardio toxicity the potential for drugs and other substances to cause damage to the heart has become a significant concern in modern medicine. With the increasing use of chemotherapy agents, targeted therapies, and even some commonly prescribed medications, healthcare professionals and researchers are striving to better comprehend and mitigate this adverse effect. Cardio toxicity can manifest as various cardiac complications, ranging from mild dysfunction to life-threatening conditions such as heart failure and arrhythmias. This article aims to provide an overview of cardio toxicity, its causes, mechanisms, and current approaches to prevention and management. Cardio toxicity can be broadly classified into two main types: Type I and Type II. Type I cardio toxicity is characterized by direct, dose-dependent damage to the heart muscle. Examples include anthracyclines, such as doxorubicin, commonly used in cancer treatment.

Keywords

Cardio toxicity, Doxorubicin, Acetylation, Oxidative stress, Programmed cell death, Reactive Oxygen species.

Introduction

These agents can induce oxidative stress, disrupt cellular membranes, and lead to cardiomyocyte death. Type II cardio toxicity; on the other hand, is characterized by indirect damage to the heart, typically without dose dependence. Targeted therapies, such as tyrosine kinase inhibitors (TKIs), can cause this type of toxicity by interfering with signalling pathways involved in cardiac homeostasis. Several mechanisms contribute to cardio toxicity. Oxidative stress, a state of imbalance between free radicals and antioxidants, plays a crucial role in the development of both Type I and Type II cardio toxicity.[1,2].

Oxidative stress can damage cellular components, including lipids, proteins, and DNA, leading to cellular dysfunction and death. Additionally, inflammation and immune responses triggered by drug-induced injury can exacerbate cardio toxic effects. Mitochondrial dysfunction is another key mechanism in cardio toxicity. Mitochondria are vital for energy production in cardiac cells, and impairment of mitochondrial function can lead to cellular energy depletion and compromised cardiac performance. Efforts to prevent and manage cardio toxicity involve various strategies. Cardio protective agents, such as dexrazoxane, have been developed to mitigate the toxic effects of anthracyclines in cancer patients. These agents act by chelating iron and reducing oxidative stress. Close monitoring of cardiac function through regular screenings, including echocardiography and biomarker assessments, is crucial, particularly during and after treatment with potentially cardio toxic drugs. Advancements in cardiac imaging techniques have also aided in early detection and monitoring of cardio toxicity [3].

Cardiac magnetic resonance imaging (MRI) can assess cardiac function, detect subtle changes in tissue structure, and provide valuable information about the extent and severity of cardio toxicity. Additionally, an increased understanding of genetic predisposition to cardio toxicity has led to the development of pharmacogenomics approaches. Genetic testing can identify patients at higher risk of developing cardio toxicity, enabling personalized treatment plans and dosage adjustments. Research is on-going to identify novel therapeutic targets to prevent or mitigate cardio toxicity. For instance, the use of cardio protective agents, such as beta-blockers and angiotensin-converting enzyme (ACE) inhibitors, has shown promising results in some cases. Furthermore, emerging therapies like stem cell transplantation and gene therapy hold potential in repairing damaged cardiac tissue and improving cardiac function [4,5].

Conclusion

Cardio toxicity remains a significant concern in modern medicine due to its potential impact on patients' cardiovascular health. Understanding the mechanisms of cardio toxicity, implementing preventive strategies, and adopting advanced monitoring techniques are key to reducing its incidence and managing its effects. On-going research and personalized approaches offer hope for better outcomes in the future.

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