Publications by authors named "Minzi Qiu"

Objectives: This study aims to explore the relationship of serum calcium (Ca) concentration with diabetic kidney disease (DKD) and all-cause mortality among type 2 diabetes mellitus (T2DM) patients using National Health and Nutrition Examination Surveys (NHANES).

Methods: Data of T2DM patients aged ≥ 40 years were screened from the NHANES database from 1999 to 2018. The outcomes were the risk of DKD diagnosed by urine albumin-to-creatinine ratio (UACR) ≥ 30 mg/g or estimated glomerular filtration rate (eGFR) < 60 mL/min/1.

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Disparities in socioeconomic status (SES) are associated with an increased risk of cardiovascular disease (CVD). Depression is a highly prevalent cardiovascular risk factor among individuals with low SES. The present study aimed to gain a better understanding of the association between SES and CVD by examining the mediating effects of depression.

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Background: Chronic kidney disease (CKD) lacks effective treatments and renal fibrosis (RF) is one of CKD's outcomes. Dickkopf 3 (DKK3) has been identified as an agonist in CKD. However, the underlying mechanisms of DKK3 in CKD are not fully understood.

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Chronic kidney disease (CKD) affects more than 10% of people worldwide and is a leading cause of death. However, the pathogenesis of CKD remains elusive. The oxidative stress and mitochondrial membrane potential were detected using Enzyme-linked immunosorbent assay and JC-1 assay.

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Background: Immune response plays a vital role in the initiation and development of chronic kidney disease (CKD). Detailed mechanisms and specific immune-related biomarkers of CKD need further clarification. We aimed to identify and characterize immune-related infiltrates that are implicated in the CKD development using a bioinformatics method.

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Oxidative stress and fibrosis may accelerate the progression of chronic kidney disease (CKD). DKK3 is related to regulating renal fibrosis and CKD. However, the molecular mechanism of DKK3 in regulating oxidative stress and fibrosis during CKD development has not been clarified, which deserves to be investigated.

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A high-salt diet can aggravate oxidative stress, and renal fibrosis the brain and renal renin-angiotensin system (RAS) axis in chronic kidney disease (CKD) rats. (Pro)renin receptor (PRR) plays a role in regulating RAS and oxidative stress locally. However, whether central PRR regulates salt-induced renal injury in CKD remains undefined.

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The diabetes mellitus has posed a grave threat on human health, and is bound to result in renal trauma by uncertain mechanisms. Increasing evidences indicated that the activation of the renin-angiotensin system plays a pivotal role during the progression of diabetic kidney disease. In streptozotocin (STZ)-induced type 1 diabetic rat model, the losartan (a selective angiotensin II type 1 (AT1) receptor antagonist) and tempol (4-Hydroxy-TEMPO, reactive oxygen species scavenger) were administrated through intracerebroventricular injection or intragastric gavage.

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The renoprotective effects of hypoxia inducible-factor (HIF) activators have been demonstrated by improving renal hypoxia in chronic kidney disease. Cobalt chloride is one of the most widely used HIF activators in biomedicine; however, poor kidney targeting and undesirable side effects greatly limit its clinical applications. Here, we report a novel stimuli-responsive drug release nanoplatform in which glutathione (GSH)-modified Au nanoparticles (GLAuNPs) and Co2+ self-assemble into nanoassemblies (GLAuNPs-Co) through coordination interactions between empty orbitals of Co2+ and lone pairs of GSH.

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Article Synopsis
  • The study investigates the role of distal cerebrospinal fluid-contacting nucleus (dCSF-CNs) in chronic kidney disease (CKD) progression, proposing that their ablation could mitigate kidney damage by affecting the renin-angiotensin system (RAS).
  • Rats underwent a procedure (5/6 nephrectomy) to model CKD, with some subjected to dCSF-CNs ablation, which was confirmed through immunofluorescence staining.
  • Results showed that dCSF-CNs ablation led to decreased levels of harmful RAS components and inflammatory markers, while improving beneficial ones, suggesting a potential therapeutic target for renal inflammation and fibrosis in CKD.
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Background: The tumor suppressor PTEN serves as a negative regulator of PI3K/PTEN/Akt signaling pathway that regulates cellular functions such as cell growth, differentiation, proliferation and migration. The PI3K/PTEN/Akt signaling cascades might also have effect on glucose uptake via translocation of GLUT-4. Insulin controls energy storage and the whole body glucose homeostasis.

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Hypothalamic paraventricular nucleus (PVN) is a cardiovascular regulating center within the brain, which plays a critical role in high salt-induced progression of chronic renal failure (CRF). However, the phosphoproteomic changes in the PVN caused by CRF remain unclear. This study aimed to perform large-scale phosphoproteomic analysis of PVN induced by CRF and high salt intake.

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The central nervous system plays a vital role in the development of hypertension, but the molecular regulatory mechanisms are not fully understood. This study aimed to explore signaling in the paraventricular nucleus (PVN) which might contribute to renal hypertension. Renal hypertension model was established by five-sixth nephrectomy operation (5/6Nx) in male Sprague Dawley rats.

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Objective: To investigate the effects of advanced oxidation protein products (AOPP) on epithelial-to-mesenchymal transition (EMT) in cultured human proximal tubular epithelial cells (HK-2) and explore the mechanism.

Methods: HK-2 cells treated with 50, 100, 200, and 400 µg/ml AOPP or 50 µg/m bovine serum albumin (BSA) for 24 h, or with 200 µg/ml AOPP for 0.5, 1, 3, 6, 12, and 24 h were examined for the protein expression of α-SMA and E-cadherin.

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Objective: To investigate the association between single nucleotide polymorphisms (SNPs) of the transmembrane protein 39A (TMEM39A) at the loci 1880G/A, 2442T/G, and 2456A/T and systemic lupus erythematosus (SLE) in Chinese Han patients.

Methods: TMEM39A gene polymorphisms at 3 loci (1880G/A, 2442T/G, 2456 A/T) were analyzed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in 110 Chinese Han patients with SLE and 80 normal control subjects, and the allele and genotype frequencies were compared by Chi-square test between the two groups.

Results: Both the genotype frequencies (AA, GA and GG) and allele frequencies (A and G) at 1880G/A differed significantly between SLE cases and the normal controls (P=0.

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