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

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

ORGANISM(S): Mus musculus

PROVIDER: GSE322779 | GEO | 2026/05/11

REPOSITORIES: GEO

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