Abstract
Disorders of uric acid metabolism may be associated with pathological processes in many diseases, including diabetes mellitus, cardiovascular disease, and kidney disease. These diseases can further promote uric acid accumulation in the body, leading to a vicious cycle. Preliminary studies have proven many mechanisms such as oxidative stress, lipid metabolism disorders, and rennin angiotensin axis involving in the progression of hyperuricaemia-related diseases. However, there is still lack of effective clinical treatment for hyperuricaemia. According to previous research results, NPT1, NPT4, OAT1, OAT2, OAT3, OAT4, URAT1, GLUT9, ABCG2, PDZK1, these urate transports are closely related to serum uric acid level. Targeting at urate transporters and urate-lowering drugs can enhance our understanding of hyperuricaemia and hyperuricaemia-related diseases. This review may put forward essential references or cross references to be contributed to further elucidate traditional and novel urate-lowering drugs benefits as well as provides theoretical support for the scientific research on hyperuricemia and related diseases.
Highlights
With lifestyle changes, hyperuricaemia has become common around the world. 85–90% of hyperuricaemia patients have no clinical features
The results of this study shows that: 1) based on the serum levels of urate salt gene, the lack of SLC22A12 was 10% more prominent in men than in women, and can be genetic (Misawa et al, 2020); 2) based on urate absorption, some of the variants truncate a protein that may have a termination codon that leads to the loss of URAT1 function (Cha et al, 2019)
NPT1, NPT4, ABCG2 expressed on the apical membrane and OAT1, OAT3 expressed on the basolateral membrane have been confirmed to contribute to the secretory transport of urate from proximal tubular epithelial cells into the tubule lumen (Cleophas et al, 2017)
Summary
Hyperuricaemia has become common around the world. 85–90% of hyperuricaemia patients have no clinical features. Urate transporters are mostly located in the proximal tubules of the kidney and play key roles in reabsorption and excretion of UA. Previous studies indicate that reduced SUA levels in the body can lead to an increased risk of Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, schizophrenia, and dementia (Ascherio et al, 2009; Du et al, 2016; Ye et al, 2016) These findings may be associated with the antioxidant effects that UA may display in neurodegenerative diseases (Tana et al, 2018). One of the main causes of hyperuricaemia is not true overproduction of UA, but insufficient excretion of extra renal UA due to common ABCG2 dysfunction (Ichida et al, 2012) It exerts active roles in patients with CKD (Yano et al, 2014; Nigam, 2015; Bhatnagar et al, 2016). Clinical studies have shown that PF-06743649 causes a large and rapid decrease in serum uric acid in healthy subjects and gout patients (Yue et al, 2019)
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