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The molecular basis of myocardial hypertrophy and heart failure
1Department of Medicine, University of Wuerzburg, Josef Schneider Strasse 2, 97080 Wuerzburg, Germany.
Insights
Heart failure (HF) occurs when the heart cannot meet the body's metabolic demands, progressing due to factors like kidney retention and neurohumoral activation. This review clarifies HF terminology and focuses on the failing heart's gene program changes and molecular mechanisms.
Area of Science:
- Cardiology
- Molecular Biology
- Physiology
Background:
- Heart failure (HF) represents the common end-stage of numerous cardiac diseases.
- HF is characterized by relentless progression and the heart's inability to meet peripheral metabolic demands.
- Key progression mechanisms involve renal retention, neurohumoral activation, and cardiac gene expression alterations.
Purpose of the Study:
- To clarify confusing terminology associated with heart failure.
- To provide an overview of peripheral mechanisms contributing to HF.
- To focus on the molecular mechanisms and gene program changes in the failing heart.
Main Methods:
- Review of existing literature on heart failure mechanisms.
- Analysis of molecular and genetic alterations in cardiac tissue during HF.
- Explanation of neurohumoral and renal factors influencing HF progression.
Main Results:
- The review elucidates the complex terminology surrounding heart failure.
- Peripheral mechanisms including renal sodium/water retention and neurohumoral activation are discussed.
- Significant alterations in the heart's gene program and underlying molecular mechanisms are detailed.
Conclusions:
- Understanding the molecular basis of HF is crucial for developing novel treatments.
- The review provides insights into the progression of heart failure at the molecular level.
- This knowledge aids in comprehending recent therapeutic strategies for heart failure.
Abstract:
Heart failure (HF) is the inability of the heart to cope with the metabolic demands of the periphery. It is the common end-stage of many frequent cardiac diseases and is characterized by relentless progression. Mechanisms of progression include renal sodium and water retention, neurohumoral activation and alterations of the protein composition (gene programme) of the heart itself. In this review, we explain the often confusing terminology in the subject, briefly touch upon the peripheral mechanisms of HF, and then focus on the changes in the gene programme of the failing heart and the molecular mechanisms leading to them. Understanding the basic processes underlying HF will help uninitiated readers to gain insight into recent novel approaches to its treatment.