Publications by authors named "Jing-Hong Zhao"

Background: Renal fibrosis is key histopathological lesion in chronic kidney disease progression. This study explored pyroptosis-related gene signatures, potential molecular pathways and chemicals, as well as immune infiltration in renal fibrosis.

Methods: Renal fibrosis datasets and pyroptosis-related genes were obtained and differentially expressed pyroptosis-related genes (DEPGs) were identified.

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Introduction: Although recent research suggests that alterations in gut microbiota play a critical role in the pathophysiology of kidney diseases, the causal relationship between specific intestinal flora and the risk of kidney diseases remains unclear. Here, we investigated the causal relationship between gut microbiota and different kidney diseases through mendelian randomization analysis.

Methods: Gut microbiota and three types of kidney diseases, including diabetic nephropathy, IgA nephropathy, and membranous nephropathy, were identified from large-scale genome-wide association studies summary data.

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Purpose: The association between vitamin E and the risk of kidney disease is well documented in observational studies, but the role of vitamin E in kidney disease remain inconclusive. Here, we evaluated the causal effect of vitamin E on the risk of multiple kidney diseases, including chronic kidney disease, membranous nephropathy, diabetic nephropathy, IgA nephropathy, and dialysis.

Methods: We conducted a two-sample Mendelian randomization analysis from large-scale trans-ancestry genome-wide association studies to determine whether there was a significant causal relationship between vitamin E and multiple kidney diseases in European, American, and Asian ancestry.

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Objectives: The study aims to identify the outcome and the related factors of unvaccinated patients with end-stage kidney disease during the Omicron pandemic.

Design: A multicentre retrospective study of patients with end-stage kidney disease undergone maintenance haemodialysis (HD) in China.

Setting: 6 HD centres in China.

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Background: The association between bone morphogenetic protein 10 (BMP10) and atrial fibrillation (AF) has been widely investigated by observational studies, but their causal relationships remain inconclusive. Here, we aimed to evaluate the causal effect of BMP10 on the risk of AF through single-nucleotide polymorphisms.

Methods: A Mendelian randomization (MR) analytic framework was applied to data from two BMP10-specific genome-wide association studies comprising a total of 11,036,163 single-nucleotide polymorphisms of European ancestry.

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Wang, Si-Yang, Jun Liang, and Jing-Hong Zhao. A Case of High-Altitude Renal Syndrome. 00:000-000, 2024.

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Background: The essential roles of platelets in thrombosis have been well recognized. Unexpectedly, thrombosis is prevalent during thrombocytopenia induced by cytotoxicity of biological, physical and chemical origins, which could be suffered by military personnel and civilians during chemical, biological, radioactive, and nuclear events. Especially, thrombosis is considered a major cause of mortality from radiation injury-induced thrombocytopenia, while the underlying pathogenic mechanism remains elusive.

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Background: Whether guided antiplatelet therapy in patients with acute coronary syndrome (ACS) is effective in improving net clinical benefits compared with conventional antiplatelet therapy remains controversial. Therefore, we assessed the safety and efficacy of guided antiplatelet therapy in patients with ACS and undergoing percutaneous coronary intervention.

Method: We searched PubMed, EMBASE, and Cochrane Library databases to select the relevant randomized controlled trials comparing the guided and conventional antiplatelet therapy in patients with ACS.

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The hypobaric and hypoxic conditions of high-altitude areas exert adverse effects on the respiratory, circulatory and nervous systems. The kidneys have an abundant blood supply (20%-25% of cardiac output) and high blood flow; thus, they are susceptible to the effects of hypoxia. However, the effects of acute and chronic exposure to high altitudes on renal physiology and pathology are not fully understood.

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Background: Autosomal recessive polycystic kidney disease (ARPKD) is an autosomal recessive hepatorenal fibrocystic syndrome. The majority of ARPKD patients progress to end-stage renal disease. Precise molecular diagnosis of ARPKD has proven valuable for understanding its mechanism and selecting optimal therapy.

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Introduction: Restless legs syndrome (RLS) is a common neurological sensorimotor disorder among patients with end stage renal disease. This clinical trial aimed to provide evidence on the efficacy and safety of pramipexole in patients with uremic RLS receiving peritoneal dialysis (PD).

Methods And Analysis: This is a 12-week, multicentre, randomised, double-blind, placebo-controlled clinical trial.

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The main cellular constituents in glomerular mesangium are mesangial cells, which account for approximately 30-40% of the total cells in the glomerulus. Together with the mesangial matrix, mesangial cells form the glomerular basement membrane (GBM) in the glomerulus, whose main function is to perform the filtration. Under the pathologic conditions, mesangial cells are activated, leading to hyperproliferation and excess extracellular matrix (ECM).

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Cardiac fibroblasts (CFs) play a key role in cardiac fibrosis by regulating the balance between extracellular matrix synthesis and breakdown. Although phosphatase and tensin homologue on chromosome 10 (PTEN) has been found to play an important role in cardiovascular disease, it is not clear whether PTEN is involved in functional regulation of CFs. In the present study, PTEN was overexpressed in neonatal rat CFs via recombinant adenovirus-mediated gene transfer.

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The predominant transcription factors regulating key genes in diabetic kidney disease have not been established. The transcription factor upstream stimulatory factor 1 (USF1) is an important regulator of glucose-mediated transforming growth factor (TGF)-β1 expression in mesangial cells; however, its role in the development of diabetic kidney disease has not been evaluated. In the present study, wild-type (WT; USF1 +/+), heterozygous (USF1 +/-), and homozygous (USF1 -/-) knockout mice were intercrossed with Akita mice (Ins2/Akita) to induce type 1 diabetes.

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Aim: To investigate whether Smad6 and Smad7 can regulate TGF-beta-induced epithelial-mesenchymal transition in human renal proximal tubule epithelial cells.

Methods: Two recombinant adeno-associated viruses (AAV) expressing Smad6 and Smad7 genes were produced without helper virus and then they were delivered into human renal proximal tubule epithelial cells (HKCs). The cells were randomly divided into normal controls, TGF-beta1-treated group, Smad7-infected control, LacZ-infected control, TGF-beta1+Smad7 group or TGF-beta1+Smad6 group, and TGF-beta1 + LacZ group.

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Aim: To construct the adeno-associated virus(AAV) vectors of Smad 6 and Smad 7 genes and observe their expressions in human renal tubule epithelial cells.

Methods: The plasmids pcDNA3-Smad 6/flag and pcDNA3-Smad 7/flag were digested with BamH I and Xho I. Then the Smad 6/flag and Smad 7/flag gene fragments were cloned into plasmid pAAV-MCS, respectively to construct the recombinant pAAV-Smad 6/flag and pAAV-Smad 7/flag plasmids.

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