The genetic basis of gout.
Gout results from deposition of monosodium urate (MSU) crystals. Elevated serum urate concentrations (hyperuricemia) are not sufficient for the development of disease. Genome-wide association studies (GWAS) have identified 28 loci controlling serum urate levels. The largest genetic effects are seen in genes involved in the renal excretion of uric acid, with others being involved in glycolysis. Whereas much is understood about the genetic control of serum urate levels, little is known about the genetic control of inflammatory responses to MSU crystals. Extending knowledge in this area depends on recruitment of large, clinically ascertained gout sample sets suitable for GWAS.
Department of Biochemistry, University of Otago, Dunedin 9012, New Zealand. Electronic address: tony.merriman@otago.ac.nz.
Tony R
TR
Merriman
Section of Rheumatology and Clinical Epidemiology Unit, Boston University School of Medicine, Boston, MA 02118, USA.
Hyon K
HK
Choi
Department of Medicine, University of Auckland, Auckland 1023, New Zealand.
Nicola
N
Dalbeth
D059647:Gene-Environment Interaction; D055106:Genome-Wide Association Study; D006019:Glycolysis / Q000235:genetics; D006073:Gout / Q000235:genetics*; D006801:Humans; D033461:Hyperuricemia / Q000235:genetics*; D007668:Kidney / Q000378:metabolism*; D014527:Uric Acid / Q000378:metabolism*
D014527:Uric Acid
ABCG2; Association; Gene; Genome-wide association studies; Gout; SLC2A9; Urate