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VEGFR3 mitigates hypertensive nephropathy by enhancing mitophagy via regulating crotonylation of HSPA1L.
Cell Commun Signal
January 2025
Department of Cardiology, the 2nd Affiliated Hospital of Harbin Medical University, Harbin, 150001, China.
Oxidative stress-associated proximal tubular cells (PTCs) damage is an important pathogenesis of hypertensive renal injury. We previously reported the protective effect of VEGFR3 in salt-sensitive hypertension. However, the specific mechanism underlying the role of VEGFR3 in kidney during the overactivation of the renin-angiotensin-aldosterone system remains unclear.
View Article and Find Full Text PDFStructural basis for human NKCC1 inhibition by loop diuretic drugs.
EMBO J
January 2025
Department of Biochemistry, University of Utah School of Medicine, Salt Lake City, UT, 84112-5650, USA.
Na-K-Cl cotransporters functions as an anion importers, regulating trans-epithelial chloride secretion, cell volume, and renal salt reabsorption. Loop diuretics, including furosemide, bumetanide, and torsemide, antagonize both NKCC1 and NKCC2, and are first-line medicines for the treatment of edema and hypertension. NKCC1 activation by the molecular crowding sensing WNK kinases is critical if cells are to combat shrinkage during hypertonic stress; however, how phosphorylation accelerates NKCC1 ion transport remains unclear.
View Article and Find Full Text PDFTargeted modulation of intestinal barrier and mucosal immune-related microbiota attenuates IgA nephropathy progression.
Gut Microbes
December 2025
State Key Laboratory of Bioreactor Engineering, East China University of Science and Technology, Shanghai, China.
IgA nephropathy (IgAN) is related to the balance of gut microbiota. However, it is unclear whether changes in the gut microbiota can cause IgAN or attenuate its progression. This study employed IgAN and human microbiota-associated (HMA)-IgAN models to investigate the impact of IgAN on gut microbiota alteration and the mechanisms by which gut microbiota might trigger IgAN.
View Article and Find Full Text PDFRenal and Peripheral Blood Transcriptome Signatures That Predict Treatment Response in Proliferative Lupus Nephritis-A Prospective Study.
Immunology
January 2025
Department of Clinical Immunology, Jawaharlal Institute of Post-Graduate Medical Education and Research (JIPMER), Puducherry, India.
Mechanisms contributing to non-response to treatment in lupus nephritis (LN) are unclear. We characterised the transcriptome of paired peripheral blood mononuclear cells (PBMCs) and renal tissues in LN before and after cyclophosphamide (CYC) treatment and identified markers that predicted treatment response. Total RNA isolated from paired PBMCs (n = 32) and renal tissues (n = 25) of 16 proliferative LN before CYC treatment, 6 months post-treatment, and during renal flare, was sequenced on Illumina Novaseq-6000 platform.
View Article and Find Full Text PDFSex differences in aristolochic acid I-induced nephrotoxicity in mice and the effect of estradiol.
Toxicol Appl Pharmacol
January 2025
School of Pharmacy, Southwest Medical University, Luzhou, Sichuan 646000, China; Luzhou New Drug Evaluation and Research Center, Luzhou, Sichuan 646000, China. Electronic address:
Aristolochic acid I (AAI), the most prominent component of aristolochic acids and found in nearly all aristolochic herbs, has been demonstrated significant nephrotoxicity. In this study, an acute nephrotoxicity model of AAI mice was established by a single dose injection of AAI. It was observed that there are differences of the sensitivity to AAI nephrotoxicity in female and male mice, with male mice exhibiting nephrotoxic effects even at lower doses.
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