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Omics · study · 2026

Transcription factor TFEB antagonizes cardiac hypertrophy and failure by enhancing lysosomal capacity and mitochondrial function

Listed in NCBI GEO

Pathological cardiac remodeling and increased afterload-driven demand contribute to heart failure.

Description

TFEB is a key regulator of lysosomal genes and mitochondrial function and is activated in response to external stress. To elucidate TFEB-dependent transcriptional programs under hypertrophic stress, we profiled left ventricular transcriptomes from a cardiomyocyte-specific TFEB knockout mouse model subjected to transverse aortic constriction (TAC) or sham surgery, with wild-type littermate controls, followed by downstream multi-omics integration.

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From keywords
Life Sciences
Inferred from text
Cardiac remodeling 75% · Heart 75%
Provenance · 1 source records, 9 field assertions
SourceKeyLast seenRaw
NCBI GEOGSE32277911 d agoJSON v1
FieldAssertionExtractorEvidence
access_levelsource · NCBI GEOconnector:ncbi_geo@1.0.0
concepts[anatomy].local:anatomy:heartenrichment · NCBI GEOkeyword-concept-rules@1.0.0title+description (75%)
concepts[disease].local:disease:cardiac-remodelingenrichment · NCBI GEOkeyword-concept-rules@1.0.0title+description (75%)
concepts[field].local:field:life-sciencesmapping · NCBI GEOconnector:ncbi_geo@1.0.0
concepts[method].geo_series_type:expression-profiling-by-high-throughput-sequencingsource · NCBI GEOconnector:ncbi_geo@1.0.0/gdstype
concepts[organism].NCBITaxon:10090source · NCBI GEOconnector:ncbi_geo@1.0.0/taxon
descriptionsource · NCBI GEOconnector:ncbi_geo@1.0.0/summary
publication_datesource · NCBI GEOconnector:ncbi_geo@1.0.0
titlesource · NCBI GEOconnector:ncbi_geo@1.0.0/title