208 results match your criteria preventing podocyte


Evolutionary conservation of intrinsically unstructured regions in slit-diaphragm proteins.

PLoS One 2021 21;16(7):e0254917. Epub 2021 Jul 21.

Department of Biochemistry, School of Life Sciences, University of Hyderabad, Hyderabad, India.

Vertebrate kidneys contribute to homeostasis by regulating electrolyte, acid-base balance, removing toxic metabolites from blood, and preventing protein loss into the urine. Glomerular podocytes constitute the blood-urine barrier, and podocyte slit-diaphragm (SD), a modified tight junction, contributes to the glomerular permselectivity. Nephrin, KIRREL1, podocin, CD2AP, and TRPC6 are crucial members of the SD that interact with each other and contribute to the SD's structural and functional integrity. Read More

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CLEC14A protects against podocyte injury in mice with adriamycin nephropathy.

FASEB J 2021 07;35(7):e21711

Department of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, China.

Podocyte injury is a major determinant of focal segmental glomerular sclerosis (FSGS) and the identification of potential therapeutic targets for preventing podocyte injury has clinical importance for the treatment of FSGS. CLEC14A is a single-pass transmembrane glycoprotein belonging to the vascular expressed C-type lectin family. CLEC14A is found to be expressed in vascular endothelial cells during embryogenesis and is also implicated in tumor angiogenesis. Read More

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A Nephrologist Perspective on Obesity: From Kidney Injury to Clinical Management.

Front Med (Lausanne) 2021 13;8:655871. Epub 2021 Apr 13.

Nephrology Department, Vall d'Hebron University Hospital, Barcelona, Spain.

Obesity is one of the epidemics of our era. Its prevalence is higher than 30% in the U.S. Read More

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JAK/STAT pathway promotes the progression of diabetic kidney disease via autophagy in podocytes.

Eur J Pharmacol 2021 Jul 24;902:174121. Epub 2021 Apr 24.

Department of Clinical Pharmacy, The Second Aliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, PR China. Electronic address:

Diabetic kidney disease (DKD) is one of the major microvascular complications of diabetes and an important cause of end-stage renal disease. Previous studies have shown that the damage to podocyte autophagy is related to the pathogenesis of DKD, and this damage is closely mediated by the Janus kinase (JAK)/signal transductors and the transcription (STAT) signaling pathway. Here, the underlying molecular mechanism of the JAK/STAT signaling pathway regulating podocyte autophagy was investigated. Read More

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Integrin β3 overexpression contributes to podocyte injury through inhibiting RhoA/YAP signaling pathway.

Bioengineered 2021 12;12(1):1138-1149

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

Axis formed by integrin β3 (ITGβ3)-Ras homolog gene family, member A (RhoA), and Yes-associated protein (YAP) plays an important role in atherosclerosis. In addition, ITGβ3 overexpression was noted in high-glucose (HG) exposure podocytes. However, the ITGβ3-RhoA-YAP axis on HG-induced podocyte injury remains unclear. Read More

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December 2021

Deficiency of Mitochondrial Glycerol 3-Phosphate Dehydrogenase Exacerbates Podocyte Injury and the Progression of Diabetic Kidney Disease.

Diabetes 2021 Jun 19;70(6):1372-1387. Epub 2021 Mar 19.

Department of Endocrinology, Translational Research of Diabetes Key Laboratory of Chongqing Education Commission of China, The Second Affiliated Hospital of Army Medical University, Chongqing, China

Mitochondrial function is essential for bioenergetics, metabolism, and signaling and is compromised in diseases such as proteinuric kidney diseases, contributing to the global burden of kidney failure, cardiovascular morbidity, and death. The key cell type that prevents proteinuria is the terminally differentiated glomerular podocyte. In this study, we characterized the importance of mitochondrial glycerol 3-phosphate dehydrogenase (mGPDH), located on the inner mitochondrial membrane, in regulating podocyte function and glomerular disease. Read More

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Combination CTLA-4 immunoglobulin treatment and ultrasound microbubble-mediated exposure improve renal function in a rat model of diabetic nephropathy.

Aging (Albany NY) 2021 03 10;13(6):8524-8540. Epub 2021 Mar 10.

Department of Ultrasonic Diagnosis, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325027, Zhejiang, China.

Objective: This study explored the therapeutic impact of combined cytotoxic T lymphocyte-associated antigen 4 immunoglobulin (CTLA-4-Ig) treatment and microbubble-mediated exposure in a rat model of diabetic nephropathy (DN).

Method: We treated rats using CTLA-4-Ig and/or microbubble exposure. At 8 weeks post-intervention, key parameters were evaluated including blood biochemistry, damage to renal tissue, renal parenchymal elasticity, ultrastructural changes in podocytes, and renal parenchymal expression of CD31, CD34, IL-6, Fn, Collagen I, Talin, Paxillin, α3β1, podocin, nephrin, and B7-1. Read More

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Xanthine oxidoreductase inhibitor topiroxostat ameliorates podocyte injury by inhibiting the reduction of nephrin and podoplanin.

Nefrologia (Engl Ed) 2021 Mar 8. Epub 2021 Mar 8.

Department of Cell Biology, Kidney Research Center, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan. Electronic address:

Background: Topiroxostat, an inhibitor of xanthine oxidoreductase (XOR) was shown to reduce urinary albumin excretion of hyperuricemic patients with chronic kidney disease. However, its pharmacological mechanism is not well understood. In this study, we examined the effects of topiroxostat on glomerular podocytes. Read More

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Disruption of pathways regulated by Integrator complex in Galloway-Mowat syndrome due to WDR73 mutations.

Sci Rep 2021 Mar 8;11(1):5388. Epub 2021 Mar 8.

Laboratory of Hereditary Kidney Diseases, Imagine Institute, INSERM UMR 1163, Université de Paris, 75015, Paris, France.

Several studies have reported WDR73 mutations to be causative of Galloway-Mowat syndrome, a rare disorder characterised by the association of neurological defects and renal-glomerular disease. In this study, we demonstrate interaction of WDR73 with the INTS9 and INTS11 components of Integrator, a large multiprotein complex with various roles in RNA metabolism and transcriptional control. We implicate WDR73 in two Integrator-regulated cellular pathways; namely, the processing of uridylate-rich small nuclear RNAs (UsnRNA), and mediating the transcriptional response to epidermal growth factor stimulation. Read More

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Calpastatin prevents Angiotensin II-mediated podocyte injury through maintenance of autophagy.

Kidney Int 2021 07 3;100(1):90-106. Epub 2021 Mar 3.

Université de Paris, PARCC, Inserm, Paris, France. Electronic address:

The strong predictive value of proteinuria in chronic glomerulopathies is firmly established as well as the pathogenic role of angiotensin II promoting progression of glomerular disease with an altered glomerular filtration barrier, podocyte injury and scarring of glomeruli. Here we found that chronic angiotensin II-induced hypertension inhibited autophagy flux in mouse glomeruli. Deletion of Atg5 (a gene encoding a protein involved autophagy) specifically in the podocyte resulted in accelerated angiotensin II-induced podocytopathy, accentuated albuminuria and glomerulosclerosis. Read More

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Management of congenital nephrotic syndrome: consensus recommendations of the ERKNet-ESPN Working Group.

Nat Rev Nephrol 2021 04 29;17(4):277-289. Epub 2021 Jan 29.

Division of Nephrology and Dialysis, Department of Pediatric Subspecialties, Bambino Gesù Pediatric Hospital Istituto di Ricerca e Cura a Carattere Scientifico (IRCCS), Rome, Italy.

Congenital nephrotic syndrome (CNS) is a heterogeneous group of disorders characterized by nephrotic-range proteinuria, hypoalbuminaemia and oedema, which manifest in utero or during the first 3 months of life. The main cause of CNS is genetic defects in podocytes; however, it can also be caused, in rare cases, by congenital infections or maternal allo-immune disease. Management of CNS is very challenging because patients are prone to severe complications, such as haemodynamic compromise, infections, thromboses, impaired growth and kidney failure. Read More

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Effects of High Glucose and Lipotoxicity on Diabetic Podocytes.

Nutrients 2021 Jan 15;13(1). Epub 2021 Jan 15.

Division of Nephrology, Endocrinology and Metabolism, Department of Internal Medicine, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.

Glomerular podocytes are highly differentiated cells that cover glomerular capillaries from the outside and have a characteristic morphology with numerous foot processes. The formation of slit membranes between the foot processes serves as a final filtration barrier for urine filtration from the blood. Podocyte damage causes disruption of the slit membrane, subsequent proteinuria and finally glomerulosclerosis, which is a common pathway in various types of chronic kidney disease (CKD). Read More

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January 2021

The Therapeutic Effect of Active Vitamin D Supplementation in Preventing the Progression of Diabetic Nephropathy in a Diabetic Mouse Model.

J Diabetes Res 2020 26;2020:7907605. Epub 2020 Nov 26.

The Diabetes & Metabolism Lab, Baruch Padeh Poriya Medical Center, Lower Galilee, Israel.

Background: Diabetic nephropathy (DN) is one of the most common microvascular complications of diabetes and is the leading cause of end-stage renal disease (ESRD) and replacement therapy worldwide. Vitamin D levels in DN patients are very low due to the decrease in the synthesis and activity of 1- hydroxylase in the proximal tubule cells and decrease in the vitamin D receptor abundance. To date, few studies have shown the antioxidant effects of 1,25-dihydroxyvitamin D [1,25(OH)D] on hyperglycemia-induced renal injury. Read More

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November 2020

Intracellular Calcium Homeostasis and Kidney Disease.

Curr Med Chem 2021 ;28(18):3647-3665

Department of Nephrology, The Third Xiangya Hospital of Central South University, Changsha 410013, Hunan Province, China.

Kidney disease is a serious health problem that burdens our healthcare system. It is crucial to find the accurate pathogenesis of various types of kidney disease to provide guidance for precise therapies for patients suffering from these diseases. However, the exact molecular mechanisms underlying these diseases have not been fully understood. Read More

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Dyslipidemia in Kidney Disorders: Perspectives on Mitochondria Homeostasis and Therapeutic Opportunities.

Front Physiol 2020 3;11:1050. Epub 2020 Sep 3.

Research and Development, Salem Veteran Affairs Medical Center, Salem, VA, United States.

To excrete body nitrogen waste and regulate electrolyte and fluid balance, the kidney has developed into an energy factory with only second to the heart in mitochondrial content in the body to meet the high-energy demand and regulate homeostasis. Energy supply from the renal mitochondria majorly depends on lipid metabolism, with programed enzyme systems in fatty acid β-oxidation and Krebs cycle. Renal mitochondria integrate several metabolic pathways, including AMPK/PGC-1α, PPARs, and CD36 signaling to maintain energy homeostasis for dynamic and static requirements. Read More

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September 2020

Synaptopodin Is Dispensable for Normal Podocyte Homeostasis but Is Protective in the Context of Acute Podocyte Injury.

J Am Soc Nephrol 2020 12 16;31(12):2815-2832. Epub 2020 Sep 16.

Division of Nephrology, Washington University School of Medicine, St. Louis, Missouri

Background: Synaptopodin (Synpo) is an actin-associated protein in podocytes and dendritic spines. Many functions in regulating the actin cytoskeleton RhoA and other pathways have been ascribed to Synpo, yet no pathogenic mutations in the gene have been discovered in patients. Naturally occurring Synpo isoforms are known (Synpo-short and -long), and a novel truncated version (Synpo-T) is upregulated in podocytes from mutant mice. Read More

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December 2020

Histone Deacetylases Take Center Stage on Regulation of Podocyte Function.

Kidney Dis (Basel) 2020 Jul 29;6(4):236-246. Epub 2020 Apr 29.

The Key Laboratory of Infection and Immunity of Shandong Province, Department of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, China.

Background: Podocytes (highly specialized and terminally differentiated epithelial cells) are integral components of the glomerular filtration barrier that are vulnerable to a variety of injuries and, as a result, they undergo a series of changes ranging from hypertrophy to detachment and apoptosis. Podocyte injury is a major determinant in proteinuric kidney disease and identification of potential therapeutic targets for preventing podocyte injury has clinical importance. Although numerous studies have achieved dramatic advances in the understanding of podocyte biology and its relevance to renal injury, few effective and specific therapies are available. Read More

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(Pro)renin receptor decoy peptide PRO20 protects against adriamycin-induced nephropathy by targeting the intrarenal renin-angiotensin system.

Am J Physiol Renal Physiol 2020 11 31;319(5):F930-F940. Epub 2020 Aug 31.

Department of Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City, Utah.

Adriamycin (ADR) administration in susceptible rodents such as the BALB/c mouse strain produces injury to the glomerulus mimicking human chronic kidney disease due to primary focal segmental glomerulosclerosis. The goal of the present study was to use this model to investigate antiproteinuric actions of the (pro)renin receptor decoy inhibitor PRO20. BALB/c mice were pretreated for 1 day with PRO20 at 500 μg·kg·day via an osmotic minipump followed by a single injection of vehicle or ADR (10 mg/kg) via the tail vein. Read More

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November 2020

The Emerging Role of Vitamin D and Vitamin D Receptor in Diabetic Nephropathy.

Biomed Res Int 2020 11;2020:4137268. Epub 2020 Jul 11.

Department of Nephrology, The First Affiliated Hospital of Zhengzhou University, 1 East Jianshe Road, Zhengzhou, Henan 450052, China.

Diabetic nephropathy (DN), one of the most common and severe microvascular complications of diabetes mellitus (DM), is an important risk factor for DM patient's death. Nowadays, DN has become the leading cause of end-stage renal disease (ESRD) in most countries without effective therapeutic methods. Recently, the renoprotective effects mediated by vitamin D (VD) and vitamin D receptor (VDR) have been evidenced. Read More

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The mechanisms of ameliorating effect of a green tea polyphenol on diabetic nephropathy based on diacylglycerol kinase α.

Sci Rep 2020 07 16;10(1):11790. Epub 2020 Jul 16.

Department of Applied Chemistry in Bioscience, Graduate School of Agricultural Science, Kobe University, Rokkodai-Cho 1-1, Nada-Ku, Kobe, 657-8501, Japan.

Significant efforts have been made to ameliorate diabetic nephropathy (DN) by inhibiting protein kinase C. However, these efforts have not been successful in human trials, suggesting that novel therapeutic strategies are required. Thus far, it has been reported that green tea polyphenol epigallocatechin gallate (EGCg) improved albuminuria in DN in a human trial. Read More

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Baicalin serves a protective role in diabetic nephropathy through preventing high glucose-induced podocyte apoptosis.

Exp Ther Med 2020 Jul 29;20(1):367-374. Epub 2020 Apr 29.

Department of Pharmacy, Hospital Affiliated 5 to Nantong University, Taizhou People's Hospital, Taizhou, Jiangsu 225300, P.R. China.

Diabetic nephropathy (DN) is one of the late complications of diabetes, which seriously affects the lives of patients. Baicalin (BA) is a flavone glycoside that has been identified to improve renal function in patients with DN. The present study aimed to investigate the roles and mechanisms of BA in DN. Read More

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Glomerular Transcriptome Profiles in Focal Glomerulosclerosis: New Genes and Pathways for Steroid Resistance.

Am J Nephrol 2020 29;51(6):442-452. Epub 2020 Apr 29.

Department of Nephrology, Institute of Nephrology, Shanghai Ruijin Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, China.

Background: Patients with focal segmental glomerulosclerosis (FSGS) characterized by steroid-resistant nephrotic syndrome (SRNS) are prone to progress to ESRD. Mechanism for the FSGS patients' response to steroid treatment is still unknown and currently, it is impossible to predict the steroid resistance before treatment of patients with FSGS.

Methods: To identify biomarkers and potential therapeutic targets of FSGS patients with SRNS, patients diagnosed as kidney biopsy-proven FSGS and nephrotic syndrome (NS) were prospectively enrolled. Read More

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From protein uptake to Dent disease: An overview of the CLCN5 gene.

Gene 2020 Jul 11;747:144662. Epub 2020 Apr 11.

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

Proteinuria is a well-known risk factor, not only for renal disorders, but also for several other problems such as cardiovascular diseases and overall mortality. In the kidney, the chloride channel Cl/H exchanger ClC-5 encoded by the CLCN5 gene is actively involved in preventing protein loss. This action becomes evident in patients suffering from the rare proximal tubulopathy Dent disease because they carry a defective ClC-5 due to CLCN5 mutations. Read More

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Immunization with Pentraxin3 prevents transition from subclinical to clinical lupus nephritis in lupus-prone mice: Insights from renal ultrastructural findings.

J Autoimmun 2020 07 4;111:102443. Epub 2020 Apr 4.

Unit of Rheumatology, Department of Medicine (DIMED), University of Padova, Padova, Italy. Electronic address:

Background: Pentraxin3 (PTX3) is an emerging player in lupus nephritis (LN). Anti-PTX3 antibodies showed to delay LN occurrence in vivo.

Aim: To evaluate renal changes following immunization with PTX3 in a murine model of LN. Read More

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Reconsidering Garth Robinson: fluid flow and the glomerular filtration barrier.

Curr Opin Nephrol Hypertens 2020 05;29(3):273-279

Nephrology and Hypertension, Vanderbilt University Medical Center, Nashville, Tennessee, USA.

Purpose Of Review: The goal of this review is to present recent models of the filtration barrier that may suggest mechanism-based treatments for proteinuric renal disease. The vast majority of renal failure occurs in diseases of glomerular proteinuria. The physiology of the filtration barrier remains incompletely understood, preventing invention of mechanism-based therapies. Read More

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APOL1 C-Terminal Variants May Trigger Kidney Disease through Interference with APOL3 Control of Actomyosin.

Cell Rep 2020 03;30(11):3821-3836.e13

Laboratory of Molecular Parasitology, IBMM, Université Libre de Bruxelles, 6041 Gosselies, Belgium. Electronic address:

The C-terminal variants G1 and G2 of apolipoprotein L1 (APOL1) confer human resistance to the sleeping sickness parasite Trypanosoma rhodesiense, but they also increase the risk of kidney disease. APOL1 and APOL3 are death-promoting proteins that are partially associated with the endoplasmic reticulum and Golgi membranes. We report that in podocytes, either APOL1 C-terminal helix truncation (APOL1Δ) or APOL3 deletion (APOL3KO) induces similar actomyosin reorganization linked to the inhibition of phosphatidylinositol-4-phosphate [PI(4)P] synthesis by the Golgi PI(4)-kinase IIIB (PI4KB). Read More

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Glomerular podocytes in diabetic renal disease.

Adv Clin Exp Med 2019 Dec;28(12):1711-1715

Voivodeship Specialty Hospital, Center for Research and Development, Wrocław, Poland.

Diabetic nephropathy (DN) is the most common cause of end-stage renal disease (ESRD), both in the USA and in Europe; moreover, its incidence is rising worldwide. The main laboratory markers of DN progression are albuminuria and a reduction in glomerular filtration rates, although progression of the disease has been observed even in the absence of these biomarkers. Renal impairment, associated with diabetes, results from damage to the glomerular filtration barrier, at the level of highly differentiated glomerular epithelial cells: podocytes. Read More

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December 2019

Podocyte GSK3α is important for autophagy and its loss detrimental for glomerular function.

FASEB Bioadv 2019 Aug 1;1(8):498-510. Epub 2019 Jul 1.

Bristol Renal, University of Bristol.

Podocytes are key cells in maintaining the integrity of the glomerular filtration barrier and preventing albuminuria. Glycogen synthase kinase 3 (GSK3) is a multi-functional serine/threonine kinase existing as two distinct but related isoforms (α and β). In the podocyte it has previously been reported that inhibition of the β isoform is beneficial in attenuating a variety of glomerular disease models but loss of both isoforms is catastrophic. Read More

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NLRP3 inflammasome negatively regulates podocyte autophagy in diabetic nephropathy.

Biochem Biophys Res Commun 2020 01 6;521(3):791-798. Epub 2019 Nov 6.

College of Basic Medical, Binzhou Medical University, Yantai, Shandong, China. Electronic address:

Inflammasome mechanisms are recognized as a key pathophysiology of diabetic nephropathy (DN). The nucleotide-oligomerization domain-like receptor 3 (NLRP3) inflammasome has attracted the most attention. Autophagy as a conserved intracellular catabolic pathway plays essential roles in the maintenance of podocytes. Read More

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January 2020

Focal segmental glomerulosclerosis ACTN4 mutants binding to actin: regulation by phosphomimetic mutations.

Sci Rep 2019 10 29;9(1):15517. Epub 2019 Oct 29.

Departments of Pathology, University of Pittsburgh, Pittsburgh, PA, 15213, USA.

Natural mutations such as lysine 255 to glutamic acid (K to E), threonine 259 to isoleucine (T to I) and serine 262 to proline (S to P) that occur within the actin binding domain of alpha-actinin-4 (ACTN4) cause an autosomal dominant form of focal segmental glomerulosclerosis (FSGS) in affected humans. This appears due to elevated actin binding propensity in podocytes resulting in a 'frozen' cytoskeleton. What is challenging is how this cellular behavior would be compatible with other cell functions that rely on cytoskeleton plasticity. Read More

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October 2019