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RAAS and adrenergic genes in heart failure: Function, predisposition and survival implications
Alberto J Alves1, Nir Eynon, José Oliveira
1Alberto J Alves, José Oliveira, The Research Centre in Physical Activity, Health and Leisure, University of Porto, Faculty of Sport, 4200-450 Porto, Portugal.
World Journal of Cardiology
|December 17, 2010
Summary
Common gene variants in the renin-angiotensin-aldosterone system (RAAS) and adrenergic system do not typically predispose individuals to heart failure. However, specific single nucleotide polymorphisms (SNPs) impact drug responses and survival in heart failure patients.
Area of Science:
- Cardiovascular Medicine
- Genetics
- Pharmacology
Background:
- Neurohormonal and signaling pathways, including the renin-angiotensin-aldosterone system (RAAS) and adrenergic system, are implicated in heart failure pathogenesis.
- Genetic variations in these systems may influence heart failure progression and outcomes, but existing research presents conflicting findings.
Purpose of the Study:
- To review the impact of single nucleotide polymorphisms (SNPs) in genes of the RAAS and adrenergic system on heart failure predisposition and survival.
- To clarify the role of specific genetic variants in modulating heart failure course and response to therapy.
Main Methods:
- Literature review of studies investigating the association between common SNPs in RAAS and adrenergic system genes and heart failure.
- Analysis of data on predisposition, pharmacological responses, and survival outcomes related to specific SNPs.
Main Results:
- Most common SNPs in RAAS and adrenergic system genes do not appear to predispose individuals to heart failure.
- Specific SNPs, including ARB1 Arg389Gly, GRK5 Gln41Leu, ACE I/D, CYP11B2 C-344T, and AGTR1 A+1166C, significantly affect pharmacological responses and cardiac survival.
Conclusions:
- While common SNPs may not directly cause heart failure, certain variants influence patient outcomes and treatment efficacy.
- Future research should explore gene-gene interactions and environmental factors in homogeneous populations to better understand heart failure pathogenesis and survival.
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