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| http://dx.doi.org/10.3389/fendo.2015.00145 | DOI Listing |
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High mobility group box 1 (HMGB1) mediates nicotine-induced podocyte injury.
Front Pharmacol
January 2025
Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX, United States.
Introduction: Cigarette smoking is a well-established risk factor for renal dysfunction. Smoking associated with renal damage bears distinct physiological correlations in conditions such as diabetic nephropathy and obesity-induced glomerulopathy. However, the cellular and molecular basis of such an association remains poorly understood.
View Article and Find Full Text PDFVascular injury in glomerulopathies: the role of the endothelium.
Front Nephrol
December 2024
Renal Pathophysiology Laboratory, Hospital das Clínicas, University of São Paulo School of Medicine, São Paulo, Brazil.
In glomerulopathies, endothelial dysfunction and the presence of histological vascular lesions such as thrombotic microangiopathy, arteriolar hyalinosis, and arteriosclerosis are related to a severe clinical course and worse renal prognosis. The endothelial cell, which naturally has anti-inflammatory and anti-thrombotic regulatory mechanisms, is particularly susceptible to damage caused by various etiologies and can become dysfunctional due to direct/indirect injury or a deficiency of protective factors. In addition, endothelial regulation and protection involve participation of the complement system, factors related to angiogenesis, the renin-angiotensin system (RAS), endothelin, the glycocalyx, the coagulation cascade, interaction between these pathways, interactions between glomerular structures (the endothelium, mesangium, podocyte, and basement membrane) and interstitial structures (tubules, arterioles and small vessels).
View Article and Find Full Text PDFProteinuria and proximal tubular epithelial cells: correlation between immunofluorescence, histology, and degree of proteinuria.
Front Nephrol
October 2024
Department of Pathology, The Ohio State University Wexner Medical Center, Columbus, OH, United States.
Article Synopsis
- Proteins are filtered from blood by the glomerular filtration barrier and then reabsorbed by proximal tubular epithelial cells (PTECs), which create tubular protein reabsorption droplets (TPRDs) from these proteins.
- A study analyzing 109 kidney biopsies found a negative correlation between albumin TPRDs and proteinuria, while positive correlations were observed between proteinuria and IgG TPRDs and acute tubular necrosis (ATN).
- The findings suggest that healthy PTECs are crucial for managing protein levels in urine, as their effectiveness declines with conditions like ATN, leading to increased proteinuria.
Barleriside A, an aryl hydrocarbon receptor antagonist, ameliorates podocyte injury through inhibiting oxidative stress and inflammation.
Front Pharmacol
August 2024
School of Pharmacy, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
Introduction: Increasing evidence shows that hyperactive aryl hydrocarbon receptor (AHR) signalling is involved in renal disease. However, no currently available intervention strategy is effective in halting disease progression by targeting the AHR signalling. Our previous study showed that barleriside A (BSA), a major component of , exhibits renoprotective effects.
View Article and Find Full Text PDFTHSD7A-associated membranous nephropathy involves both complement-mediated and autonomous podocyte injury.
Front Pharmacol
July 2024
Division of Nephrology, Department of Medicine, Toledo, OH, United States.
Membranous nephropathy (MN) continues to be a leading cause of nephrotic syndrome in non-diabetic adults. As a unique subtype in the serology-based classification of MN, thrombospondin type 1 domain containing 7A (THSD7A)-associated MN has attracted increasing interest, because, unlike other autoantigens, THSD7A is also expressed in preclinical species, facilitating the study of its role in MN. A heterologous mouse model of THSD7A-associated MN was previously established using a proprietary in-house antibody that was unfortunately not available to the research community.
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