230 results match your criteria podocytes promoter


The AGE receptor, OST48 drives podocyte foot process effacement and basement membrane expansion (alters structural composition).

Endocrinol Diabetes Metab 2021 Jul 22;4(3):e00278. Epub 2021 Jun 22.

Glycation and Diabetes Complications Mater Research Institute - The University of Queensland Translational Research Institute Woolloongabba Qld Australia.

Aims: The accumulation of advanced glycation end products is implicated in the development and progression of diabetic kidney disease. No study has examined whether stimulating advanced glycation clearance via receptor manipulation is reno-protective in diabetes. Podocytes, which are early contributors to diabetic kidney disease and could be a target for reno-protection. Read More

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Homocysteine induces podocyte apoptosis by regulating miR-1929-5p expression through c-Myc, DNMT1 and EZH2.

Mol Oncol 2021 May 31. Epub 2021 May 31.

School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, China.

Chronic kidney disease (CKD) is a common and complex disease in kidneys which has been associated with an increased risk of renal cell carcinoma. Elevated homocysteine (Hcy) levels are known to influence the development and progression of CKD by regulating podocyte injury and apoptosis. To investigate the molecular mechanisms triggered in podocytes by Hcy, we used cbs mice and observed that higher Hcy levels increased the apoptosis rate of podocytes with accompanying glomerular damage. Read More

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Receptor activator of NF-κB mediates podocyte injury in diabetic nephropathy.

Kidney Int 2021 Aug 27;100(2):377-390. Epub 2021 May 27.

Department of Nephrology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, China.

Receptor activator of NF-κB (RANK) expression is increased in podocytes of patients with diabetic nephropathy. However, the relevance of RANK to diabetic nephropathy pathobiology remains unclear. Here, to evaluate the role of podocyte RANK in the development of diabetic nephropathy, we generated a mouse model of podocyte-specific RANK depletion (RANKCre T), and a model of podocyte-specific RANK overexpression (RANK TG), and induced diabetes in these mice with streptozotocin. Read More

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DACH1 protects podocytes from experimental diabetic injury and modulates PTIP-H3K4Me3 activity.

J Clin Invest 2021 May;131(10)

Division of Nephrology, Icahn School of Medicine at Mount Sinai, New York, New York, USA.

Dachshund homolog 1 (DACH1), a key cell-fate determinant, regulates transcription by DNA sequence-specific binding. We identified diminished Dach1 expression in a large-scale screen for mutations that convert injury-resistant podocytes into injury-susceptible podocytes. In diabetic kidney disease (DKD) patients, podocyte DACH1 expression levels are diminished, a condition that strongly correlates with poor clinical outcomes. Read More

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scRNA Transcription Profile of Adult Zebrafish Podocytes Using a Novel Reporter Strain.

Cell Physiol Biochem 2021 May;55(S4):35-47

Queen's Medical Research Institute, Cardiovascular Science Centre, University of Edinburgh, Edinburgh, UK.

Background/aims: The role of podocytes is well conserved across species from drosophila to teleosts, and mammals. Identifying the molecular markers that actively maintain the integrity of the podocyte will enable a greater understanding of the changes that lead to damage.

Methods: We generated transgenic zebrafish, expressing fluorescent reporters driven by the podocin promoter, for the visualization and isolation of podocytes. Read More

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Sp1-mediated upregulation of Prdx6 expression prevents podocyte injury in diabetic nephropathy via mitigation of oxidative stress and ferroptosis.

Life Sci 2021 Aug 21;278:119529. Epub 2021 Apr 21.

Department of Endocrinology, Shuyang People's Hospital, The Affiliated Shuyang Hospital of Xuzhou Medical University, China.

Glomerular podocyte damage is considered to be one of the main mechanisms leading to Diabetic nephropathy (DN). However, the relevant mechanism of podocyte injury is not yet clear. This study aimed to investigate the effect of peroxiredoxin 6 (Prdx6) on the pathogenesis of podocyte injury induced by high glucose (HG). Read More

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Vitamin D and Glomerulonephritis.

Medicina (Kaunas) 2021 Feb 22;57(2). Epub 2021 Feb 22.

Unit of Nephrology and Dialysis, Department of Clinical and Experimental Medicine, University of Messina, 98125 Messina, Italy.

Vitamin D presents a plethora of different functions that go beyond its role in skeletal homeostasis. It is an efficient endocrine regulator of the Renin-Angiotensin-Aldosterone System (RAAS) and erythropoiesis, exerts immunomodulatory effects, reduces the cardiovascular events and all-cause mortality. In Chronic Kidney Disease (CKD) patients, Vitamin D function is impaired; the renal hydrolyzation of its inactive form by the action of 1α-hydroxylase declines at the same pace of reduced nephron mass. Read More

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February 2021

APOL1 risk variants affect podocyte lipid homeostasis and energy production in focal segmental glomerulosclerosis.

Hum Mol Genet 2021 Apr;30(3-4):182-197

Katz Family Division of Nephrology and Hypertension, Department of Medicine, University of Miami Miller School of Medicine, Miami, Florida 33136, USA.

Lipotoxicity was recently reported in several forms of kidney disease, including focal segmental glomerulosclerosis (FSGS). Susceptibility to FSGS in African Americans is associated with the presence of genetic variants of the Apolipoprotein L1 gene (APOL1) named G1 and G2. If and how endogenous APOL1 may alter mitochondrial function by the modifying cellular lipid metabolism is unknown. Read More

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Transcription factor Kruppel-like factor 5 positively regulates the expression of AarF domain containing kinase 4.

Mol Biol Rep 2020 Nov 8;47(11):8419-8427. Epub 2020 Oct 8.

Department of Pediatrics, The First Affiliated Hospital, Nanjing Medical University, Nanjing, 210029, Jiangsu, China.

AarF domain containing kinase 4 (ADCK4) is identified as a candidate gene associated with hereditary nephrotic syndrome (NS). Kruppel-like factor 5 (KLF5) is reported to promote podocyte survival by blocking the ERK/p38 MAPK pathways. Both ADCK4 and KLF5 are involved in the occurrence and development of podocyte disease, but their interaction remains unclear. Read More

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November 2020

WT1 activates transcription of the splice factor kinase SRPK1 gene in PC3 and K562 cancer cells in the absence of corepressor BASP1.

Biochim Biophys Acta Gene Regul Mech 2020 12 2;1863(12):194642. Epub 2020 Oct 2.

Centre for Research in Bioscience, Faculty of Health and Applied Sciences, University of the West of England, Coldharbour Lane, Frenchay, Bristol BS16 1QY, United Kingdom. Electronic address:

Dysregulated alternative splicing plays a prominent role in all hallmarks of cancer. The splice factor kinase SRPK1 drives the activity of oncogenic splice factors such as SRSF1. SRSF1 in turn promotes the expression of splice isoforms that favour tumour growth, including proangiogenic VEGF. Read More

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December 2020

Calcineurin inhibitors ameliorate PAN-induced podocyte injury through the NFAT-Angptl4 pathway.

J Pathol 2020 11 8;252(3):227-238. Epub 2020 Sep 8.

Kidney Disease Center, The First Affiliated Hospital, College of Medicine, Zhejiang University; Key Laboratory of Kidney Disease Prevention and Control Technology, Zhejiang Province; National Key Clinical Department of Kidney Diseases; Institute of Nephrology, Zhejiang University; The Third Grade Laboratory under the National State, Administration of Traditional Chinese Medicine, Hangzhou, PR China.

Podocyte injury plays a vital role in proteinuria and nephrotic syndrome. Calcineurin (CaN) inhibitors are effective in reducing proteinuria. However, their molecular mechanism is still not fully understood. Read More

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November 2020

Role of SIRT1 in HIV-associated kidney disease.

Am J Physiol Renal Physiol 2020 08 13;319(2):F335-F344. Epub 2020 Jul 13.

Division of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.

Human immunodeficiency virus (HIV) infection of kidney cells can lead to HIV-associated nephropathy (HIVAN) and aggravate the progression of other chronic kidney diseases. Thus, a better understanding of the mechanisms of HIV-induced kidney cell injury is needed for effective therapy against HIV-induced kidney disease progression. We have previously shown that the acetylation and activation of key inflammatory regulators, NF-κB p65 and STAT3, were increased in HIVAN kidneys. Read More

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MYDGF attenuates podocyte injury and proteinuria by activating Akt/BAD signal pathway in mice with diabetic kidney disease.

Diabetologia 2020 09 25;63(9):1916-1931. Epub 2020 Jun 25.

The First School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong Province, China.

Aims/hypothesis: Myeloid-derived growth factor (MYDGF), mainly secreted by bone marrow-derived cells, has been known to promote glucagon-like peptide-1 production and improve glucose/lipid metabolism in mouse models of diabetes, but little is known about the functions of MYDGF in diabetic kidney disease (DKD). Here, we investigated whether MYDGF can prevent the progression of DKD.

Methods: In vivo experiments, both loss- and gain-of-function strategies were used to evaluate the effect of MYDGF on albuminuria and pathological glomerular lesions. Read More

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September 2020

Absence of Long Noncoding RNA H19 Promotes Childhood Nephrotic Syndrome through Inhibiting ADCK4 Signal.

Med Sci Monit 2020 Jun 3;26:e922090. Epub 2020 Jun 3.

Department of Pediatrics and Nephrology, Wuxi Children's Hospital Affiliated to Nanjing Medical University, Wuxi, Jiangsu, China (mainland).

BACKGROUND Nephrotic syndrome (NS) is a common chronic kidney disease in children characterized by a group of clinical symptoms such as massive proteinuria, hypoproteinemia, high edema, and hyperlipidemia. Despite the tremendous efforts already made, the diagnosis for nephrotic syndrome still remains poor in children. MATERIAL AND METHODS The blood samples from 30 healthy children and 30 children with nephrotic syndrome were collected. Read More

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The Krüppel-like factor 15-NFATc1 axis ameliorates podocyte injury: a novel rationale for using glucocorticoids in proteinuria diseases.

Clin Sci (Lond) 2020 06;134(12):1305-1318

Department of Nephrology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangdong Provincial Institute of Geriatrics, Guangzhou, 510080, China.

Podocyte injury and loss contribute to proteinuria, glomerulosclerosis and eventually kidney failure. Recent studies have demonstrated that the loss of Kruppel-like factor 15 (KLF15) in podocytes increases the susceptibility to injury; however, the mechanism underlying the protective effects on podocyte injury remains incompletely understood. Herein, we showed that KLF15 ameliorates podocyte injury through suppressing NFAT signaling and the salutary effects of the synthetic glucocorticoid dexamethasone in podocyte were partially mediated by the KLF15-NFATc1 axis. Read More

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Role for carbohydrate response element-binding protein (ChREBP) in high glucose-mediated repression of long noncoding RNA Tug1.

J Biol Chem 2020 11 28;295(47):15840-15852. Epub 2020 May 28.

Section of Nephrology, Division of Internal Medicine, The University of Texas at MD Anderson Cancer Center, Houston, Texas, USA; Department of Pharmacology & Chemical Biology, Baylor College of Medicine, Houston, Texas, USA. Electronic address:

Long noncoding RNAs (lncRNAs) have been shown to play key roles in a variety of biological activities of the cell. However, less is known about how lncRNAs respond to environmental cues and what transcriptional mechanisms regulate their expression. Studies from our laboratory have shown that the lncRNA Tug1 (taurine upregulated gene 1) is crucial for the progression of diabetic kidney disease, a major microvascular complication of diabetes. Read More

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November 2020

MiR193a Modulation and Podocyte Phenotype.

Cells 2020 04 17;9(4). Epub 2020 Apr 17.

Institute of Molecular Medicine, Feinstein Institute for Medical Research and Zucker School of Medicine at Hofstra-North well, New York, NY 11030, USA.

Apolipoprotein L1 (APOL1)-miR193a axis has been reported to play a role in the maintenance of podocyte homeostasis. In the present study, we analyzed transcription factors relevant to miR193a in human podocytes and their effects on podocytes' molecular phenotype. The motif scan of the miR193a gene provided information about transcription factors, including YY1, WT1, Sox2, and VDR-RXR heterodimer, which could potentially bind to the miR193a promoter region to regulate miR193a expression. Read More

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5'UTR isoforms in human kidneys: differential expression analysis between controls and patients with glomerulonephritis.

J Investig Med 2020 04 3;68(4):864-869. Epub 2020 Feb 3.

Kidney Histomorphology and Molecular Biology Laboratory, Clinical Nephrology Unit, Department of Medicine-DIMED, University of Padua, Padua, Italy.

ClC-5, the electrogenic chloride/proton exchanger strongly expressed in renal proximal tubules, belongs to the endocytic macromolecular complex responsible for albumin and low-molecular-weight protein uptake. ClC-5 was found to be overexpressed in glomeruli of glomerulonephritis and in cultured human podocytes under albumin overload. The transcriptional regulation of human ClC-5 is not fully understood. Read More

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Notch4 activation aggravates NF-κB-mediated inflammation in HIV-1-associated nephropathy.

Dis Model Mech 2019 12 17;12(12). Epub 2019 Dec 17.

Department of Internal Medicine, University of Kansas Medical Center, Kansas City, KS 66160, USA

Notch pathway activation plays a central role in the pathogenesis of many glomerular diseases. We have previously shown that Notch4 expression was upregulated in various renal cells in human immunodeficiency virus (HIV)-associated nephropathy (HIVAN) patients and rodent models of HIVAN. In this study, we examined whether the Notch pathway can be distinctly activated by HIV-1 gene products and whether Notch4, in particular, can influence disease progression. Read More

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December 2019

tRNA-derived fragments (tRFs) contribute to podocyte differentiation.

Biochem Biophys Res Commun 2020 01 16;521(1):1-8. Epub 2019 Oct 16.

Department of Pediatric Nephrology, 2nd Affiliated Hospital of Nanjing Medical University, Nanjing, 210003, China. Electronic address:

Loss of glomerular podocytes is the crucial event in the progression of chronic kidney disease (CKD). tRNA-derived fragments (tRFs), a newfangled branch of small non-coding RNA (sncRNA), recently reported to play a vital part in several diseases. In present study, we aimed to detect and reveal the role of tRFs in podocyte differentiation. Read More

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January 2020

Evidence for miR-548c-5p regulation of FOXC2 transcription through a distal genomic target site in human podocytes.

Cell Mol Life Sci 2020 Jun 17;77(12):2441-2459. Epub 2019 Sep 17.

Molecular Medicine Research Center and Department of Biological Sciences, University of Cyprus, Nicosia, Cyprus.

Podocytes are highly differentiated epithelial cells outlining the glomerular vessels. FOXC2 is a transcription factor essential for inducing podocyte differentiation, development and maturation, and is considered to be the earliest podocyte marker. miRNA prediction analysis revealed a full-length target site for the primate-specific miR-548c-5p at a genomic region > 8 kb upstream of FOXC2. Read More

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Genetic Deletion of Does Not Cause Proteinuric Kidney Disease in Mice.

Front Med (Lausanne) 2019 27;6:189. Epub 2019 Aug 27.

Division of Nephrology and Hypertension, Feinberg Cardiovascular and Renal Research Institute, Northwestern University Feinberg School of Medicine, Chicago, IL, United States.

Nephrotic syndrome is one of the most common glomerular diseases in children and can be classified on the basis of steroid responsiveness. While multiple genetic causes have been discovered for steroid resistant nephrotic syndrome, the genetics of steroid sensitive nephrotic syndrome remains elusive. Mutations in Epithelial Membrane Protein 2 (), a member of the GAS3/PMP22 tetraspan family of proteins, were recently implicated as putative monogenic cause of steroid sensitive nephrotic syndrome. Read More

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Silencing of long noncoding RNA PVT1 inhibits podocyte damage and apoptosis in diabetic nephropathy by upregulating FOXA1.

Exp Mol Med 2019 08 1;51(8):1-15. Epub 2019 Aug 1.

Department of Nephrology, The First Affiliated Hospital of Zhengzhou University, 450052, Zhengzhou, China.

The number of patients with diabetic nephropathy (DN) is still on the rise worldwide, and this requires the development of new therapeutic strategies. Recent reports have highlighted genetic factors in the treatment of DN. Herein, we aimed to study the roles of long noncoding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) and histone 3 lysine 27 trimethylation (H3K27me3) in DN. Read More

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Gut microbial metabolite butyrate protects against proteinuric kidney disease through epigenetic- and GPR109a-mediated mechanisms.

FASEB J 2019 11 31;33(11):11894-11908. Epub 2019 Jul 31.

Nephrology Division, Department of Medicine, Universidade Federal de São Paulo, São Paulo, Brazil.

Butyrate is a short-chain fatty acid derived from the metabolism of indigestible carbohydrates by the gut microbiota. Butyrate contributes to gut homeostasis, but it may also control inflammatory responses and host physiology in other tissues. Butyrate inhibits histone deacetylases, thereby affecting gene transcription, and also signals through the metabolite-sensing G protein receptor (GPR)109a. Read More

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November 2019

Triptolide preserves glomerular barrier function via the inhibition of p53-mediated increase of GADD45B.

Arch Biochem Biophys 2019 08 19;671:210-217. Epub 2019 Jul 19.

National Clinical Research Center of Kidney Diseases, Jinling Hospital, Nanjing University School of Medicine, Nanjing, 210016, China. Electronic address:

Podocytes are important to glomerular filtration barrier integrity and maintenance of size selectivity in protein filtration in the kidney. Although there is evidence to suggest that triptolide has direct protective effects on podocyte injuries, the mechanism mediating this process remains largely unexplored. In this study, we found triptolide suppresses podocyte p53 and GADD45B expression in vivo and in vitro. Read More

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Decreased H3K9ac level of KLF4 mediates podocyte developmental toxicity induced by prenatal caffeine exposure in male offspring rats.

Toxicol Lett 2019 Oct 12;314:63-74. Epub 2019 Jul 12.

Department of Pharmacology, Basic Medical School of Wuhan University, Wuhan 430071, China; Hubei Provincial Key Laboratory of Developmentally Originated Disorder, Wuhan 430071, China. Electronic address:

This study aimed to verify the toxic effects of prenatal caffeine exposure (PCE) on the podocyte development in male offspring, and to explore the underlying intrauterine programming mechanisms. The pregnant rats were administered with caffeine (30 to 120 mg/kg⋅d) during gestational day (GD) 9 to 20. The male fetus on GD20 and the offspring at postnatal week (PW) 6 and PW28 were sacrificed. Read More

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October 2019

-254C>G SNP in the Gene Promoter Influences Its Expression via Interaction with the NF-B Subunit RELA in Steroid-Resistant Nephrotic Syndrome Children.

Int J Genomics 2019 10;2019:2197837. Epub 2019 Jun 10.

Department of Nephrology and Rheumatology, Shanghai Children's Hospital, Children's Hospital of Shanghai Jiao Tong University, Shanghai, China.

This study is aimed at exploring the mechanism by which the -254C>G single nucleotide polymorphism (SNP) on the transient receptor potential cation channel 6 () gene promoter could increase its activation in steroid-resistant nephrotic syndrome children of China. Plasmids containing the promoter region (with the -254C or G allele) were constructed and then transfected into human embryonic kidney (HEK) 293T cells and human podocytes. Luciferase assays were used to test the promoter activity in both cell lines with or without tumor necrosis factor- (TNF-) treatment, and chromatin immunoprecipitation-polymerase chain reaction (ChIP-PCR) analysis was used to verify the transcription factor that could bind to this mutant sequence. Read More

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Histone demethylase KDM6B regulates human podocyte differentiation .

Biochem J 2019 06 26;476(12):1741-1751. Epub 2019 Jun 26.

Central Laboratory, Peking University Shenzhen Hospital, Shenzhen 518036, China

Podocytes are terminally differentiated and highly specialized glomerular cells, which have an essential role as a filtration barrier against proteinuria. Histone methylation has been shown to influence cell development, but its role in podocyte differentiation is less understood. In this study, we first examined the expression pattern of histone demethylase KDM6B at different times of cultured human podocytes We found that the expression of KDM6B and podocyte differentiation markers WT1 and Nephrin are increased in the podocyte differentiation process. Read More

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The motor protein Myo1c regulates transforming growth factor-β-signaling and fibrosis in podocytes.

Kidney Int 2019 07 4;96(1):139-158. Epub 2019 Mar 4.

Department of Medicine, Nephrology Division, Medical University of South Carolina, Charleston, South Carolina, USA. Electronic address:

Transforming growth factor-β (TGF-β) is known to play a critical role in the pathogenesis of many progressive podocyte diseases. However, the molecular mechanisms regulating TGF-β signaling in podocytes remain unclear. Using a podocyte-specific myosin (Myo)1c knockout, we demonstrate whether Myo1c is critical for TGF-β-signaling in podocyte disease pathogenesis. Read More

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A KDM6A-KLF10 reinforcing feedback mechanism aggravates diabetic podocyte dysfunction.

EMBO Mol Med 2019 05;11(5)

Departments of Nephrology, Chang Gung Memorial Hospital, Chiayi, Taiwan

Diabetic nephropathy is the leading cause of end-stage renal disease. Although dysfunction of podocytes, also termed glomerular visceral epithelial cells, is critically associated with diabetic nephropathy, the mechanism underlying podocyte dysfunction still remains obscure. Here, we identify that KDM6A, a histone lysine demethylase, reinforces diabetic podocyte dysfunction by creating a positive feedback loop through up-regulation of its downstream target KLF10. Read More

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