Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Telomere recapping via gene therapy as a therapeutic strategy for cardio-renal syndromes type 4

ABSTRACT: Cardio-renal syndromes type 4 (CRS4) is defined as heart failure driven by chronic kidney disease (CKD). Cardiovascular mortality is the leading cause of mortality in advanced CKD patients. Current medical treatments exhibit limited efficacy. This study demonstrates that telomere shortening in cardiomyocytes is characteristic of CRS4. We engineered an adeno-associated virus9 (AAV9) gene therapy overexpressing catalytic inactive and nuclear localized human telomerase reverse transcriptase (modhTERT) under cardiac troponin T (cTnT) promotor. Overexpression of modhTERT recapped myocardial telomeres, reversed cardiac dysfunction, cardiac hypertrophy, cardiac fibrosis and mitochondrial dysfunction in two CRS4 animal models: 5/6 nephrectomy and Angiotensin II-high salt-uninephrectomy murine models.

ORGANISM(S): Mus musculus

PROVIDER: GSE278517 | GEO | 2026/01/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Up-regulation of prolactin receptor in the proximal tubular cells in cardio-renal syndrome model mice

Project description:The precise physiological mechanisms of cardio-renal syndrome are yet to be elucidated. In order to investigate the molecular basis of cardio-renal syndrome, we established a mouse model for cardio-renal syndrome by the combination of abdominal aortic banding and uninephrectomy. Renal function of the cardio-renal syndrome mice was synergistically decreased compared with that of mice that underwent uninephrectomy alone. To investigate the molecules involved in the deterioration renal function in the AbNx mice, we conducted comprehensive gene expression analysis using DNA array by comparing the molecules expressed in the remained kidney of AbNx mice with those of Nx mice. We conducted abdominal aorta banding or sham operation at 0 week, then We conducted uninephrectomy or sham operation at 2 week. We removed these kidney 6week after the uninephrectomy. These RNA samples were purified from the homogenized kidneys.

2012-03-19 | E-GEOD-36591 | biostudies-arrayexpress

Up-regulation of prolactin receptor in the proximal tubular cells in cardio-renal syndrome model mice

2012-03-19 | GSE36591 | GEO

5/6 nephrectomy (5/6Nx) effect on the cardiac ventricle in mouse

Project description:Chronic kidney disease (CKD) is a very important problem in global health treatment. CKD increases the disease risk of apoplexy, cardiac failure and cardiac infarction. Cardiovascular disease is especially the most serious problem. In this study, the expression of mRNA in the cardiac ventricre prepared from 5/6 nephrectomy (5/6Nx) mouse was investigated.

2020-10-05 | GSE150094 | GEO

Targeting myeloid-PCSK9 enhancing cardio-protection beyond LDL cholesterol-lowering

Project description:Circulating Proprotein Convertase Subtilisin/Kexin type 9 (PCSK9) levels, known for regulating plasma cholesterol by degrading LDL receptors, correlate with acute myocardial infarction (AMI) risk. Recent studies suggest that PCSK9 improves cardiac function beyond LDL cholesterol levels after cardiac ischemic injury, but the precise role of PCSK9 in this process is not clarified yet. Our study reveals that PCSK9 deficiency induces heterogeneous changes in myeloid cells and macrophages, potentially protecting the heart in AMI regardless of LDL cholesterol homeostasis. Single-cell RNA sequencing identifies PCSK9-dependent cardiac macrophages (PDCMs) as reparative macrophages enriched in activator protein-1 (AP-1) transcription factor (TF)-related pathways. PDCMs enhance VEGF-C secretion and activate Akt signalling in cardiac endothelial cells, improving cardiac remodelling. Indeed, PCSK9 inhibitor-treated coronary artery disease (CAD) patients show increased myeloid cells with PDCM-like features. In sum, targeting myeloid-PCSK9 may offer cardio-protective effects through increased AP-1 activity and VEGF-C expression, providing a novel approach to prevent cardiac dysfunction in AMI.

2025-07-01 | GSE285004 | GEO

5/6 nephrectomy (5/6Nx) effect on the splenic monocytes in mouse

Project description:Chronic kidney disease (CKD) is a very important problem in global health treatment. CKD increases the disease risk of apoplexy, cardiac failure and cardiac infarction. Cardiovascular disease is especially the most serious problem. In this study, the expression of mRNA in 5/6 nephrectomy (5/6Nx) mouse splenic monocytes was investigated.

2022-07-31 | GSE135191 | GEO

5/6 nephrectomy (5/6Nx) effect on the splenic monocytes in mouse

Project description:Chronic kidney disease (CKD) is a very important problem in global health treatment. CKD increases the disease risk of apoplexy, cardiac failure and cardiac infarction. Cardiovascular disease is especially the most serious problem. In this study, the expression of mRNA in 5/6 nephrectomy (5/6Nx) mouse splenic monocytes was investigated.

2020-10-05 | GSE140706 | GEO

BCOR-regulated genes in human oculo-facio-cardio-dental syndrome

Project description:Oculo-facio-cardio-dental syndrome (OFCD) is a rare genetic disorder characterized by teeth with extremely long roots (radiculomegaly), and craniofacial, eye and cardiac abnormalities. The mutation of the transcriptional co-repressor BCOR has been identified as being responsible for oculo-facio-cardio-dental (OFCD) syndrome. Mesenchymal stem cells (MSCs) is isolated from the root apical papilla of an OFCD patient. Gene expression profiling is performed and compared between mutant MSCs and wild type MSCs. Total RNA were extracted from normal MSCs (MSCWT) and mutant MSCs (MSCO).

2009-07-23 | E-GEOD-15214 | biostudies-arrayexpress

Human cTnT fragmentation in serum

Project description:Cardiac troponin T (cTnT) is a highly cardiospecific protein commonly used in the diagnosis of acute myocardial infarction (AMI), but is subject to proteolytic degradation upon its release in the circulation. In this study, a targeted mass spectrometry assay was developed to detect peptides which are differentially present within the different degradation products. cTnT was spiked in human serum and incubated at 37 °C to induce proteolytic degradation. Isolation and fractionation of cTnT and its fragments from serum were performed using immunoprecipitation and SDS-PAGE. Bands migrating to 37 kDa (intact cTnT), 29 kDa (primary fragment), and 19, 18, and 16 kDa (secondary fragments) were excised, digested, and subsequently analysed using targeted selected ion monitoring on a UHPLC-coupled quadrupole-Orbitrap mass spectrometer. Sixteen precursor ions from a total of 11 peptides unique to cTnT were targeted. Precursor ions were detectable up until 1200 ng/L cTnT, which is a typical cTnT concentration after AMI. With tandem-MS and relative quantification, we proved the formation of cTnT fragments upon incubation in human serum and identified differentially present peptides in the fragment bands, indicative of N- and C-terminal proteolytic cleavage. These findings are of importance for the development of future cTnT assays, calibrators and quality control samples.

2016-01-19 | PXD003187 | Pride

BCOR-regulated genes in human oculo-facio-cardio-dental syndrome

2009-07-23 | GSE15214 | GEO

Oxysterol Sensing through GPR183 Triggers Endothelial Senescence and Cardio-renal Injuries via Altering Circadian Signaling in Hypertension

Project description:Background: Despite endothelial dysfunction being considered as the initial step of the development of hypertension and associated cardio-renal syndromes, effective therapeutic strategies to prevent endothelial injuries are still lacking. GPR183 is a recently identified GPCR for oxysterols and hydroxylated metabolites of cholesterol. Here, we explored a previously unappreciated role of GPR183 in hypertension and age-related cardio-renal injuries. Methods and results: Mice were treated with DOCA/Salt or AngII to induce hypertension. we found that endothelial GPR183 was significantly induced in aged or hypertensive mice, which was further confirmed in renal biopsies from elderly people or subjects with hypertensive nephropathy. In addition, we found that endothelial-specific GPR183 deletion markedly ameliorated endothelial senescence and cardio-renal injuries in hypertensive mice. Mechanistically, we found that GPR183 disrupted circadian signaling by inhibiting PER1 expression, thereby facilitating endothelial senescence and dysfunction through the cAMP/PKA/CREB signaling pathway. Importantly, pharmacological inhibition of the oxysterol-GPR183 axis by NIBR189 or Clotrimazole ameliorated endothelial senescence and cardio-renal injuries in hypertensive mice. Conclusions: GPR183 is an attractive therapeutic target for hypertension and age-related diseases. Targeting GPR183 could provide novel strategies for managing hypertension and its associated cardio-renal injuries.

2024-06-23 | GSE270175 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data