Related Experiment Videos
Genetic polymorphisms and oxidative stress in heart failure
Fadi M F Alameddine1, A Maziar Zafari
1Emory University School of Medicine, Department of Medicine, Division of Cardiology, Atlanta, GA 30322, USA.
Insights
Genetic variations influencing oxidative stress are key to understanding heart failure susceptibility and progression. This review examines polymorphisms in genes related to oxidative stress and their impact on heart failure development.
Area of Science:
- Cardiovascular Medicine
- Genetics
- Molecular Biology
Background:
- Heart failure stems from cardiovascular diseases or idiopathic dilated cardiomyopathy.
- Understanding cellular events in heart failure pathogenesis is crucial for diagnosis, prevention, and therapy.
- Genetic background research in cardiomyopathies lags behind monogenic diseases.
Purpose of the Study:
- To review current data on the role of gene polymorphisms related to oxidative stress.
- To explore the influence of these polymorphisms on heart failure susceptibility and progression.
Main Methods:
- Review of existing clinical association studies.
- Analysis of genetic polymorphisms in genes involved in oxidative stress pathways.
Main Results:
- Reactive oxygen species are significantly implicated in heart failure pathogenesis.
- Genetic polymorphisms in oxidative stress-related genes may influence heart failure risk and progression.
Conclusions:
- Oxidative stress-related gene polymorphisms are important factors in heart failure.
- Further research into these genetic variations can aid in identifying susceptible individuals and guiding therapeutic strategies.
Abstract:
Heart failure results from various known cardiovascular diseases, such as coronary artery disease, or can be the result of an idiopathic dilated cardiomyopathy. It is of utmost importance for diagnostic, preventive, and therapeutic purposes to understand the cellular events that trigger the cascade of functional and structural changes that result in the development and progression of heart failure. Progress in unraveling the genetic background in both ischemic and nonischemic cardiomyopathies has been slow compared with that for monogenic diseases, such as some forms of hypertrophic cardiomyopathy or familial dilated cardiomyopathies. It is likely that susceptibility to and risk of progression of heart failure are both influenced by many genes acting in concert or independently. Among the diverse subcellular mechanisms implicated in the pathogenesis and progression of heart failure, reactive oxygen species play a major role. The search for genetic polymorphisms in clinical association studies in order to identify genotypes susceptible to develop and affect the progression to heart failure has been the focus of many investigations over the past several years. In this review, the authors summarize the current data in support of the role of various polymorphisms of genes related to oxidative stress in the susceptibility to develop heart failure, and its progression.