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311 results for “Diabetic nephropathy”
Dataset related to article "C3a receptor blockade protects podocytes from injury in diabetic nephropathy"
<p><em>The file contains raw data related to the article "C3a receptor blockade protects podocytes from injury in diabetic nephropathy", available from <a href="https://insight.jci.org/articles/view/131849">https://insight.jci.org/articles/view/131849</a>.</em></p> <ul> <li><strong>Raw data vivo 1</strong>: evaluations of complement protein renal expression in vivo</li> <li><strong>Raw data vivo 2</strong>: evaluations of systemic and laboratory parameters in vivo</li> <li><strong>Raw data vivo 3</strong>: histological evaluation of glomerular damage in vivo</li> <li><strong>Raw data vivo 4</strong>: histological evaluation of podocyte and mitochondrial dysfunction in vivo</li> <li><strong>Raw data vitro 1</strong>: evaluations of mitochondrial functional integrity in cultured podocytes</li> <li><strong>Raw data vitro 2</strong>: western blot analyses of mitochondrial proteins in cultured podocytes</li> <li><strong>Raw data vitro 3</strong>: evaluations of mitochondrial bioenergetic changes in cultured podocytes</li> <li><strong>Raw data vitro 4</strong>: evaluations of the effect of SS-31 in cultured podocytes</li> </ul> <p> </p> <p><strong>Abstract of the manuscript</strong>:</p> <p>Renal activation of the complement system has been described in patients with diabetic nephropathy (DN), although its pathological relevance is still ill-defined. Here, we studied whether glomerular C3a, generated by uncontrolled complement activation, promotes podocyte damage, leading to proteinuria and renal injury in mice with type 2 diabetes. BTBR ob/ob mice exhibited podocyte loss, albuminuria, and glomerular injury accompanied by C3 deposits and increased C3a and C3a receptor (C3aR) levels. Decreased glomerular nephrin and α-actinin4 expression, coupled with integrin-linked kinase induction, were also observed. Treatment of DN mice with a C3aR antagonist enhanced podocyte density and preserved their phenotype, limiting proteinuria and glomerular injury. Mechanistically, ultrastructural and functional mitochondrial alterations, accompanied by downregulation of antioxidant superoxide dismutase 2 (SOD2) and increased protein oxidation, occurred in podocytes and were normalized by C3aR blockade. In cultured podocytes, C3a induced cAMP-dependent mitochondrial fragmentation. Alterations of mitochondrial membrane potential, SOD2 expression, and energetic metabolism were also found in response to C3a. Notably, C3a-induced podocyte motility was inhibited by SS-31, a peptide with mitochondrial protective effects. These data indicate that C3a blockade represents a potentially novel therapeutic strategy in DN for preserving podocyte integrity through the maintenance of mitochondrial functions.</p>
Effects of Rosiglitazone on Renal Hemodynamics and Proteinuria of Type 2 Diabetic Patients With Renal Insufficiency Due to Overt Diabetic Nephropathy
ClinicalTrials.gov study NCT00324675. IPD Sharing: Not stated. Countries: 1. Publications: 1.
The Effect of Paricalcitol Capsules on Reducing Albuminuria in Patients With Type 2 Diabetic Nephropathy Being Treated With Renin-angiotensin System Inhibitors
ClinicalTrials.gov study NCT00421733. IPD Sharing: Not stated. Countries: 10. Publications: 2.
Safety and Efficacy of Different Oral Doses of BAY94-8862 in Subjects With Type 2 Diabetes Mellitus and the Clinical Diagnosis of Diabetic Nephropathy
ClinicalTrials.gov study NCT01874431. IPD Sharing: Not stated. Countries: 23. Publications: 6.
Renoprotection in Early Diabetic Nephropathy in Pima Indians
ClinicalTrials.gov study NCT00340678. IPD Sharing: Not stated. Countries: 1. Publications: 10.
Study of the Use of Niaspan for Treatment of Dyslipidemia in Diabetic Nephropathy
ClinicalTrials.gov study NCT00108485. IPD Sharing: Not stated. Countries: 1. Publications: 5.
A Study to Evaluate the Soluble Guanylate Cyclase (sGC) Stimulator IW-1973 in Diabetic Nephropathy / Diabetic Kidney Disease as Measured by Albuminuria
ClinicalTrials.gov study NCT03217591. IPD Sharing: NO. Countries: 1. Publications: 1.
Effect of Sulodexide in Early Diabetic Nephropathy
ClinicalTrials.gov study NCT00130208. IPD Sharing: NO. Countries: 3. Publications: 1.
Patiromer in the Treatment of Hyperkalemia in Patients With Hypertension and Diabetic Nephropathy (AMETHYST-DN)
ClinicalTrials.gov study NCT01371747. IPD Sharing: Not stated. Countries: 5. Publications: 4.
VA NEPHRON-D: Diabetes iN Nephropathy Study
ClinicalTrials.gov study NCT00555217. IPD Sharing: Not stated. Countries: 2. Publications: 8.
MMP-9/NGAL Modulation by Piper Crocatum in Early Diabetic Nephropathy
ClinicalTrials.gov study NCT06676124. IPD Sharing: NO. Countries: 1. Publications: 15.
(ACORD Study) - A Study of NeoRecormon (Epoetin Beta) in Patients With Early Diabetic Nephropathy
ClinicalTrials.gov study NCT00354341. IPD Sharing: Not stated. Countries: 17. Publications: 2.
Evaluation of the Effects of Canagliflozin on Renal and Cardiovascular Outcomes in Participants With Diabetic Nephropathy
ClinicalTrials.gov study NCT02065791. IPD Sharing: Not stated. Countries: 34. Publications: 40.
ORIENT: Olmesartan Reducing Incidence of End Stage Renal Disease in Diabetic Nephropathy Trial
ClinicalTrials.gov study NCT00141453. IPD Sharing: Not stated. Countries: 2. Publications: 3.
N-Acetylcysteine and Milk Thistle for Treatment of Diabetic Nephropathy
ClinicalTrials.gov study NCT01265563. IPD Sharing: UNDECIDED. Countries: 1. Publications: 7.
Efficacy and Safety of Canagliflozin (TA-7284) in Patients With Diabetic Nephropathy
ClinicalTrials.gov study NCT03436693. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Nephropathy In Type 2 Diabetes and Cardio-renal Events
ClinicalTrials.gov study NCT00535925. IPD Sharing: Not stated. Countries: 1. Publications: 5.
Thonningianin A ameliorated renal interstitial fibrosis in diabetic nephropathy mice by modulating gut microbiota dysbiosis and repressing inflammation
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Dataset related to: Endothelial Glycocalyx of Peritubular Capillaries in Experimental Diabetic Nephropathy: A Target of ACE Inhibitor-Induced Kidney Microvascular Protection
<p>The files contain all the dataset included in the manuscript divided by figures.</p> <p> </p> <p>Abstract: Peritubular capillary rarefaction is a recurrent aspect of progressive nephropathies. We previously found that peritubular capillary density was reduced in BTBR <em>ob</em>/<em>ob</em> mice with type 2 diabetic nephropathy. In this model, we searched for abnormalities in the ultrastructure of peritubular capillaries, with a specific focus on the endothelial glycocalyx, and evaluated the impact of treatment with an angiotensin-converting enzyme inhibitor (ACEi). Mice were intracardially perfused with lanthanum to visualise the glycocalyx. Transmission electron microscopy analysis revealed endothelial cell abnormalities and basement membrane thickening in the peritubular capillaries of BTBR <em>ob</em>/<em>ob</em> mice compared to wild-type mice. Remodelling and focal loss of glycocalyx was observed in lanthanum-stained diabetic kidneys, associated with a reduction in glycocalyx components, including sialic acids, as detected through specific lectins. ACEi treatment preserved the endothelial glycocalyx and attenuated the ultrastructural abnormalities of peritubular capillaries. In diabetic mice, peritubular capillary damage was associated with an enhanced tubular expression of heparanase, which degrades heparan sulfate residues of the glycocalyx. Heparanase was also detected in renal interstitial macrophages that expressed tumor necrosis factor-α. All these abnormalities were mitigated by ACEi. Our findings suggest that, in experimental diabetic nephropathy, preserving the endothelial glycocalyx is important in order to protect peritubular capillaries from damage and loss.</p>
Supplementary Table of Mechanism Unravelling of Sodium-glucose Cotransporter-2 Inhibitors against Diabetic Nephropathy via Network Pharma-cology and Molecular Docking
<p>This is the supplementary tables of article named"Mechanism Unravelling of Sodium-glucose Cotransporter-2 Inhibitors against Diabetic Nephropathy via Network Pharmacology and Molecular Docking"</p>
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