Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cerebral vascular transcriptome profiling reveals intermittent fasting modulates chronic cerebral hypoperfusion-induced disease pathways.

ABSTRACT: We investigated the effect of chronic cerebral hypoperfusion on transcriptomic changes in mouse cerebral arteries and whether intermittent fasting can modulate these transcriptomic changes.

ORGANISM(S): Mus musculus

PROVIDER: GSE246617 | GEO | 2026/07/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Cerebral vascular transcriptome profiling reveals intermittent fasting modulates chronic cerebral hypoperfusion-induced disease pathways.

Project description:Cerebral vascular transcriptome profiling reveals intermittent fasting modulates chronic cerebral hypoperfusion-induced disease pathways.

| PRJNA1033853 | ENA

Transcriptome analysis of mouse heart under different intermittent fasting conditions

Project description:Various intermittent fasting regimes are popularly being practiced but the scientific understanding for the mechanisms of intermittent fasting remains unclear. Observing the overall transcriptomic changes in specific organs, including heart, may contribute substantially in understanding the diverse effects of intermittent fasting. Our current study further investigate the differential transcriptomic changes in the heart among the different regimes of intermittent fasting as well.

2023-09-27 | GSE133290 | GEO

Transcriptome analysis reveals intermittent fasting-induced genetic changes in ischemic stroke

Project description:Intermittent fasting is previously reported to exhibit neuroprotection against experimental ischemic stroke. However, the detailed understanding of protection mechanisms are lacking. By observing the overall transcriptomic changes in each timepoint of ischemic stroke would benefit the understanding of underlying active pathways and mechanisms. Here, we conduct experimental MCAO ischemic stroke on mice exposed to different daily intermittent fasting method to compare not only among the ischemic stroke timepoints but also the efficacy of different intermittent fasting interventions. Our current study presented the transcriptomic changes for the first time in specific timepoints of ischemic stroke as well as under the condition of intermittent fasting. A number of neuroprotective mechanisms-related genes were significantly affected by intermittent fasting conditions in differential manners.

2018-07-11 | GSE116878 | GEO

Cortex-specific transcriptome profiling after deeper cerebral hypoperfusion in mice

Project description:Little is understood about the underlying cellular and molecular mechanisms related to cerebral cortex damage and glial activation after severe cerebral hypoperfusion.Efforts to explore the relationship between neuropathological and gene expression changes support a role for identifying novel molecular pathways by transcriptomic mechanisms. To investigate cortex-specific transcriptome profiling after severe cerebral hypoperfusion in mice

2023-03-09 | GSE210666 | GEO

Hippocampus-specific transcriptome profiling after severe cerebral hypoperfusion in mice

Project description:Little is understood about the underlying cellular and molecular mechanisms related to hippocampus damage and glial activation after severe cerebral hypoperfusion.Efforts to explore the relationship between neuropathological and gene expression changes support a role for identifying novel molecular pathways by transcriptomic mechanisms. To investigate hippocampus-specific transcriptome profiling after severe cerebral hypoperfusion in mice

2023-07-26 | GSE223580 | GEO

Intermittent fasting alters the spatiotemporal atlas of transcriptomes

Project description:Transcription factors may orchestrate the health benefits of intermittent fasting through directing the expression of genome. Here, we find intermittent fasting can spin the spatiotemporal profile of transcription factors, and provide an atlas of transcription factors in biological space, time and feeding regimen.

2022-10-27 | GSE154797 | GEO

Brain microvessel-specific transcriptome profiling after severe cerebral hypoperfusion in mice

Project description:Little is understood about the underlying cellular and molecular mechanisms related to brain microvessel damage and glial activation after severe cerebral hypoperfusion. Efforts to explore the relationship between neuropathological and gene expression changes support a role for identifying novel molecular pathways by transcriptomic mechanisms.

2024-12-06 | GSE266214 | GEO

Intermittent Fasting Reprograms the Brain Proteome to Prevent Synaptic Degeneration and Cognitive Impairment in Vascular Dementia

Project description:Vascular dementia (VaD), driven by chronic cerebral hypoperfusion (CCH), leads to synaptic degeneration and cognitive decline, yet mechanisms linking vascular dysfunction to synaptic loss remain unclear. Intermittent fasting (IF) has emerged as a potential intervention, but its effects on synaptic integrity in VaD are unknown. Using the bilateral common carotid artery stenosis (BCAS) mouse model, we demonstrate that a 16-hour IF regimen preserves cognitive function and cortical synaptic density despite persistent hypoperfusion. Behavioral assays revealed that IF prevented spatial memory deficits in BCAS mice, while electron microscopy confirmed synaptic preservation without altering baseline architecture. Surprisingly, synaptic protein levels remained unchanged, suggesting IF protects synaptic function rather than abundance. Proteomic profiling uncovered dynamic hippocampal adaptations under IF, including upregulation of synaptic stabilizers, enhanced GABAergic signaling, and suppression of neuroinflammatory mediators. IF also attenuated microglial engulfment of synapses, indicating modulation of complement-mediated pruning. Temporal pathway analysis revealed IF’s multi-phase neuroprotection: early synaptic reinforcement, mid-phase metabolic optimization, and late-phase suppression of chronic neuroinflammation. These findings establish IF as a potent modulator of synaptic resilience in VaD, acting through coordinated preservation of synaptic structure, inhibition of inflammatory synapse loss, and metabolic reprogramming. Our results highlight IF’s potential as a non-pharmacological strategy to combat vascular cognitive impairment by targeting the synaptic vulnerability underlying dementia progression.

2025-09-08 | PXD064537 | Pride

RNAseq of mouse corpus callosum from WT or TRPA1-KO animals under chronic cerebral hypoperfusion

Project description:Chronic cerebral hypoperfusion is manifested in various CNS diseases accompanied by cognitive impairment, such as dementia, however the precise mechanism of chronic cerebral hypoperfusion-induced cognitive impairment remains unknown. Recently, transient receptor potential ankyrin 1 (TRPA1), activated by oxidative stress, was reported to be involved in the cerebrovascular diseases, therefore we investigated the pathophysiological role of TRPA1 in chronic cerebral hypoperfusion using a mouse bilateral common carotid artery stenosis (BCAS) model. Early cognitive impairment and white matter injury was induced by BCAS in TRPA1-knockout (TRPA1-KO) but not wild-type (WT) mice. For further investigation into the involvement of TRPA1 in chronic cerebral hypoperfusion, we conducted RNA sequence (RNAseq) in the corpus callosum from sham- and BCAS-operated WT and TRPA1-KO mice.

2023-08-08 | GSE201513 | GEO

Cerebral hypoperfusion exacerbates traumatic brain injury in male mice

Project description:Traumatic brain injury (TBI) has been postulated to initiate a disease process that interacts with vascular dysfunction. However, the combined effects of preexisting cerebral hypoperfusion and TBI remain poorly explored. This study aimed to investigate the combined effects of bilateral carotid artery stenosis (BCAS) and mild-moderate TBI on cerebral blood flow (CBF), cognitive function, histology, and transcriptomics in Swiss-Webster mice. Male and female mice underwent BCAS using steel microcoils around the carotid arteries, followed by TBI 30 days post coil implantation. CBF, spatial learning and memory, axonal damage, and gene expression profiles were assessed. BCAS led to a ~10% reduction in CBF, while TBI caused a similar decrease. However, mice exposed to both BCAS and TBI exhibited more pronounced reductions in CBF, associated with marked spatial learning and memory deficits, particularly in males. Axonal damage in male mice was also exacerbated by the combination of BCAS and TBI. Notably, females demonstrated differential vascular and cognitive responses to BCAS and TBI, suggesting sex-specific protective mechanisms. Single nuclei RNA sequencing revealed unique, cell type-specific gene expression alterations due to BCAS, TBI, or the combination. Moreover, BCAS and TBI induced significant gene expression changes in various cell types, hinting at complex cellular interactions following vascular challenges and trauma. The cellular and molecular interplay between hypoperfusion and TBI points to intricate vascular-neuronal interactions and potential avenues for targeted interventions.

2024-08-14 | GSE241690 | 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