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A Review of the Epidemiological Evidence for Adducin Family Gene Polymorphisms and Hypertension
Jing Rui Zhang1, Wan Ning Hu2, Chang Yi Li1,2
1Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing 100020, China.
Insights
Essential hypertension (EH), a common cardiovascular disease, may be linked to the adducin gene family. Genetic variations in adducin may increase sodium reabsorption, contributing to hypertension development.
Area of Science:
- Cardiovascular Disease Research
- Human Genetics
- Molecular Biology
Background:
- Essential hypertension (EH) is a prevalent cardiovascular disease with unknown causes in over 95% of cases.
- High salt intake is a known risk factor for hypertension.
- Adducin, a protein complex encoded by the ADD1, ADD2, and ADD3 genes, is a candidate gene for EH.
Purpose of the Study:
- To review the structure, function, and mechanism of adducin.
- To explore the role of adducin in the onset of essential hypertension.
- To provide a basis for early screening, prevention, and treatment of EH.
Main Methods:
- Review of existing epidemiological and genetic studies.
- Analysis of animal model experiments and clinical data.
- Summary of adducin gene family structure and function.
Main Results:
- Single-nucleotide polymorphisms (SNPs) in adducin family genes may alter Na+-K+-ATPase activity.
- Increased renal tubular sodium reabsorption is suggested as a mechanism linking adducin to hypertension.
- Adducin's role in EH pathogenesis is supported by experimental and clinical evidence.
Conclusions:
- Adducin is implicated in the development of essential hypertension.
- Understanding adducin's role can aid in developing strategies for EH management.
- Further research into adducin genetics and function is warranted for targeted interventions.
Abstract:
Hypertension is one of the most common cardiovascular diseases that seriously endangers human health and has become a significant public health problem worldwide. In the vast majority of patients, the cause of hypertension is unknown, called essential hypertension (EH), accounting for more than 95% of total hypertension. Epidemiological and genetic studies of humans and animals provide strong evidence of a causal relationship between high salt intake and hypertension. Adducin is one of the important candidate genes for essential hypertension. Adducin is a heterodimeric or heterotetrameric protein that consists of α, β, and γ subunits; the three subunits are encoded by genes (ADD1, ADD2, and ADD3) that map to three different chromosomes. Animal model experiments and clinical studies suggest that changes in single-nucleotide polymorphisms (SNPs) at part of the adducin family gene increase the Na+-K+-ATPase activity of the renal tubular basement membrane and increase the reabsorption of Na+ by renal tubular epithelial cells, which may cause hypertension. This review makes a summary on the structure, function, and mechanism of adducin and the role of adducin on the onset of EH, providing a basis for the early screening, prevention, and treatment of EH.
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