The Role of ABCG2 in the Pathogenesis of Primary Hyperuricemia and Gout—An Update
Urate homeostasis in humans is a complex and highly heritable process that involves i.e., metabolic urate biosynthesis, renal urate reabsorption, as well as renal and extrarenal urate excretion. Importantly, disturbances in urate excretion are a common cause of hyperuricemia and gout. The majority o...
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| Format: | Article |
| Language: | English |
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MDPI AG
2021-06-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/22/13/6678 |
| _version_ | 1797529259225382912 |
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| author | Robert Eckenstaler Ralf A. Benndorf |
| author_facet | Robert Eckenstaler Ralf A. Benndorf |
| author_sort | Robert Eckenstaler |
| collection | DOAJ |
| description | Urate homeostasis in humans is a complex and highly heritable process that involves i.e., metabolic urate biosynthesis, renal urate reabsorption, as well as renal and extrarenal urate excretion. Importantly, disturbances in urate excretion are a common cause of hyperuricemia and gout. The majority of urate is eliminated by glomerular filtration in the kidney followed by an, as yet, not fully elucidated interplay of multiple transporters involved in the reabsorption or excretion of urate in the succeeding segments of the nephron. In this context, genome-wide association studies and subsequent functional analyses have identified the ATP-binding cassette (ABC) transporter ABCG2 as an important urate transporter and have highlighted the role of single nucleotide polymorphisms (SNPs) in the pathogenesis of reduced cellular urate efflux, hyperuricemia, and early-onset gout. Recent publications also suggest that ABCG2 is particularly involved in intestinal urate elimination and thus may represent an interesting new target for pharmacotherapeutic intervention in hyperuricemia and gout. In this review, we specifically address the involvement of ABCG2 in renal and extrarenal urate elimination. In addition, we will shed light on newly identified polymorphisms in ABCG2 associated with early-onset gout. |
| first_indexed | 2024-03-10T10:11:14Z |
| format | Article |
| id | doaj.art-f321f7ef79284633a2cc149985b771c5 |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-10T10:11:14Z |
| publishDate | 2021-06-01 |
| publisher | MDPI AG |
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| series | International Journal of Molecular Sciences |
| spelling | doaj.art-f321f7ef79284633a2cc149985b771c52023-11-22T01:12:04ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672021-06-012213667810.3390/ijms22136678The Role of ABCG2 in the Pathogenesis of Primary Hyperuricemia and Gout—An UpdateRobert Eckenstaler0Ralf A. Benndorf1Institute of Pharmacy, Martin Luther University Halle-Wittenberg, 06120 Halle, GermanyInstitute of Pharmacy, Martin Luther University Halle-Wittenberg, 06120 Halle, GermanyUrate homeostasis in humans is a complex and highly heritable process that involves i.e., metabolic urate biosynthesis, renal urate reabsorption, as well as renal and extrarenal urate excretion. Importantly, disturbances in urate excretion are a common cause of hyperuricemia and gout. The majority of urate is eliminated by glomerular filtration in the kidney followed by an, as yet, not fully elucidated interplay of multiple transporters involved in the reabsorption or excretion of urate in the succeeding segments of the nephron. In this context, genome-wide association studies and subsequent functional analyses have identified the ATP-binding cassette (ABC) transporter ABCG2 as an important urate transporter and have highlighted the role of single nucleotide polymorphisms (SNPs) in the pathogenesis of reduced cellular urate efflux, hyperuricemia, and early-onset gout. Recent publications also suggest that ABCG2 is particularly involved in intestinal urate elimination and thus may represent an interesting new target for pharmacotherapeutic intervention in hyperuricemia and gout. In this review, we specifically address the involvement of ABCG2 in renal and extrarenal urate elimination. In addition, we will shed light on newly identified polymorphisms in ABCG2 associated with early-onset gout.https://www.mdpi.com/1422-0067/22/13/6678goutearly-onset gouthyperuricemiaurateuric acidABCG2 |
| spellingShingle | Robert Eckenstaler Ralf A. Benndorf The Role of ABCG2 in the Pathogenesis of Primary Hyperuricemia and Gout—An Update International Journal of Molecular Sciences gout early-onset gout hyperuricemia urate uric acid ABCG2 |
| title | The Role of ABCG2 in the Pathogenesis of Primary Hyperuricemia and Gout—An Update |
| title_full | The Role of ABCG2 in the Pathogenesis of Primary Hyperuricemia and Gout—An Update |
| title_fullStr | The Role of ABCG2 in the Pathogenesis of Primary Hyperuricemia and Gout—An Update |
| title_full_unstemmed | The Role of ABCG2 in the Pathogenesis of Primary Hyperuricemia and Gout—An Update |
| title_short | The Role of ABCG2 in the Pathogenesis of Primary Hyperuricemia and Gout—An Update |
| title_sort | role of abcg2 in the pathogenesis of primary hyperuricemia and gout an update |
| topic | gout early-onset gout hyperuricemia urate uric acid ABCG2 |
| url | https://www.mdpi.com/1422-0067/22/13/6678 |
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