Similar Datasets
Project description:RNA-Sequencing Analysis of AVF-CKD Murine Model
| PRJNA477935 | ENA
Project description:This project involves TMT-labeled proteomics analysis of mitochondria isolated from skeletal muscle, heart, and kidney of mice with and without chronic kidney disease (CKD). CKD was induced by adenine-supplementation of the diet for 6 months. Mouse strain was C57BL6J mice from Jackson Lab, aged 6 months prior to start of the diet. Mitochondria were isolated from skeletal muscle, heart, and kidney and immediately snap frozen and stored at -80C until processing.
2021-10-06 | PXD021847 | JPOST Repository
Project description:microRNA in chronic kidney disease (CKD)
2017-01-01 | GSE80247 | GEO
Project description:Systemic iron metabolism is disrupted in chronic kidney disease (CKD). However, little is known about local kidney iron homeostasis and its role in kidney fibrosis. Kidney-specific effects of iron therapy in CKD also remain elusive. Here, we elucidate the role of macrophage iron status in kidney fibrosis and demonstrate that it is a potential therapeutic target. In CKD, kidney macrophages exhibited depletion of labile iron pool (LIP) and induction of transferrin receptor 1, indicating intracellular iron deficiency. Low LIP in kidney macrophages was associated with their defective antioxidant response and proinflammatory polarization. Repletion of LIP in kidney macrophages through knockout of ferritin heavy chain (Fth1) reduced oxidative stress and mitigated fibrosis. Similar to Fth1 knockout, iron dextran therapy, through replenishing macrophage LIP, reduced oxidative stress, decreased the production of proinflammatory cytokines, and alleviated kidney fibrosis. Interestingly, iron markedly decreased TGF-β expression and suppressed TGF-β–driven fibrotic response of macrophages. Iron dextran therapy and FtH suppression had an additive protective effect against fibrosis. Adoptive transfer of iron-loaded macrophages alleviated kidney fibrosis, validating the protective effect of iron-replete macrophages in CKD. Thus, targeting intracellular iron deficiency of kidney macrophages in CKD can serve as a therapeutic opportunity to mitigate disease progression.
2023-02-01 | GSE221598 | GEO
Project description:Urinary proteomics studies have primarily focused on identifying markers of chronic kidney disease (CKD) progression. Here, we aimed to specify CKD-related injury markers through proteomics analysis in urine of patients with CKD. Label-free quantitative proteomics analysis based on liquid chromatography-tandem mass spectrometry was performed on urine samples obtained from 6, 9, 11, and 10 patients in health control, CKD stage 1, 3 and 5, respectively.
2021-01-19 | PXD016433 | Pride
Project description:Uremic cardiomyopathy is a clinically highly relevant cause of cardiovascular events in patients with chronic kidney disease (CKD). This study aimed at a comprehensive analysis of cardiac function and cardiac pathological characteristics in adenine-induced CKD in 129/Sv mice. This included the analysis of kidney function and morphology, heart function as well as cardiac hypertrophy, fibrosis and calcification. Also, cardiac RNA-sequencing was performed. Although overall, no cardiac dysfunction, hypertrophy or fibrosis could be observed, prolonged moderate CKD in this mouse model enhanced cardiac oxidative stress markers. In line, cardiac RNA-sequencing revealed an increase in oxidative stress-inducing signaling in CKD as well as anti-inflammatory feedback responses. This suggests a maladaptive preconditioning of the heart in CKD, which could increase the risk of enhanced cardiovascular damage upon additional cardiovascular risk factors and/or events.
2022-09-21 | GSE191122 | GEO
Project description:Congenital obstructive nephropathy (CON) is the leading cause of chronic kidney disease (CKD) in children. CON is a complex disease process involving pathological changes in kidney development and function that occur as a result of obstructed antegrade urine flow beginning in utero. The megabladder (mgb-/-) mouse is an animal model of CON that develops kidney disease secondary to a bladder-specific defect in smooth muscle development. Expression levels of specific microRNAs were compared by microarray analysis on the Agilent platform and by quantitative PCR (qPCR) of kidney samples from wild type and mgb-/- mice.
2016-07-08 | GSE70879 | GEO
Project description:Genetic Study of CHronic Kidney DIsease (CKD)
| PRJNA543914 | ENA
Project description:Genetic Study of CHronic Kidney DIsease (CKD)
| PRJNA543915 | ENA
Project description:High incidence of heart failure (HF) is a typical characteristic of chronic kidney disease (CKD). However, the pathogenesis of CKD-associated HF remains elusive. Here, we investigated the changes in myocardial energy metabolism in CKD mice and explored the underlying mechanisms. To examine genome wide transcriptional changes in the heart of CKD mice, we performed microarray analysis using the Affymetrix Clariom S mouse.
2019-03-16 | GSE126824 | GEO