In this study, the expression level of miR-143-3p was significantly decreased in hyperuricemia mice model group compared with the normal control by miRNA microarray, the same results were confirmed in the hyperuricemia patients and the healthy control group.
At the molecular level, hyperuricemia was associated with decreased expression of SIRT1 and its phosphorylation, phosphorylation of FOXO3a, increased expression of AR and XO, and deacetylation of NF-κB P65.
Patients with the mixed type of HUA had the severest kidney injury manifested by a high level of 24 h urinary microalbumin, urinary immunoglobulin G, transferrin, α-galactosidase and β2-microglobulin compared with the normal uric acid group.
Our findings provide new evidence for the supplementary therapeutic potential of HAA-PSP with allopurinol on hyperuricemia and inflammation-related syndromes.
At the molecular level, hyperuricemia was associated with decreased expression of SIRT1 and its phosphorylation, phosphorylation of FOXO3a, increased expression of AR and XO, and deacetylation of NF-κB P65.
Serum concentrations of γ-HCH, o,p´-DDE, PCB-138, PCB-153, PFOA, and urinary Cadmium were associated with an increased risk of hyperuricemia, while PBDE-153 showed an inverse association with the effect.
Collectively, our results suggest that THP deficiency can cause progressive disturbances in renal functions via initially NKCC2 dysfunction and later compensatory responses, resulting in prolonged activation of the renin-angiotensin-aldosterone axis and hyperuricemia.
Importantly, RIP3-knockout mice exhibited the decrease of FAS-associated protein with a death domain (FADD), cleaved Caspase-8/-3 and Poly (ADP-ribose) polymerase (PARP) in renal samples, along with TUNEL reduction in mice with hyperuricemia.
RIP3 deficiency attenuated hyperuricemia in mice, evidenced by reduced serum uric acid and creatinine and enhanced urinary uric acid and creatinine, as well as the improved histological alterations in renal sections.
These observations support a higher intake of dietary folate, and febuxostat for losing weight to decrease NTD risk and prevent hyperuricemia and recurrent gout attacks.
As the serum uric acid, urea nitrogen, creatinine, glutamic oxalacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), superoxide dismutase (SOD), catalase (CAT) and malondialdehyde (MDA) data demonstrated, the adenine not only mediated hepatorenal function disorders, but also induced hyperuricemia in mice.
The genetic contribution to the progression from hyperuricaemia to gout remains relatively poorly understood, although genes encoding proteins that are involved in the NLRP3 (NOD-, LRR- and pyrin domain-containing 3) inflammasome pathway play a part.
We measured plasma urate and genotyped for the SLC23A1rs33972313 vitamin C variant in 106 147 individuals from the Copenhagen General Population Study, of which 24 099 had hyperuricaemia.
Hyperuricemia induction in vivo resulted in cellular apoptosis, interstitial fibrosis and diastolic dysfunction in the rat hearts, as well as increased activation of calpain-1 and endoplasmic reticulum (ER) stress, while allopurinol treatment mitigated the above changes.
Hypoadiponectinemia has been documented in patients with hyperuricemia, however, whether soluble uric acid (SUA) regulates the expression of APN and APN receptor 1 (AdipoR1) in renal proximal tubule epithelial cells (PTECs) remains to be elucidated.
Collectively, these findings suggest that the novel HES-based NP formulation of Morin may have great potential for clinical treatment of hyperuricemia.
Therefore, we propose a molecular mechanism for the induction of hyperuricemia by diuretics: the diuretics enter proximal tubular cells via basolateral OAT1 and/or OAT3 and may then interfere with the NPT4-mediated apical urate efflux in the renal proximal tubule.
Non-synonymous single nucleotide polymorphisms (SNP) loci of P2X7R in Chinese people were screened to compare the frequencies of different alleles and genotype distribution of selective SNPs in 117 gouty patients and 95 hyperuricemia patients.
The incidences of leukopenia, alopecia and liver damage were higher in the CTX group (OR (95%CI): 0.23 (0.09 to 0.59), 0.10 (0.04 to 0.24), and 0.36 (0.19 to 0.69, respectively), whereas the incidences of hirsutism, gingival hyperplasia, worsening hypertension and hyperuricemia were higher in the CSA group (OR (95%CI): 8.64 (1.97 to 37.79, 4.44 (1.09 to 17.99), 4.59 (1.43 to 14.82) and 9.05 (1.53 to 53.36), respectively).
We evaluated the association of hyperuricemia and nocturnal hypertension with lower estimated glomerular filtration rate (eGFR) using cystatin-C in patients aged 10-21 years with the HbSS or HbSB0 form of the disease during a non-acute clinic visit. eGFR and uric acid measurements were obtained in 83 and 81 participants, respectively, and 24-h ambulatory blood pressure monitoring (ABPM) was performed in 44 participants.