SPOP is a key trigger of pathological cardiac hypertrophy and heart failure

Cardiac hypertrophy is a pathological feature of heart failure, and dysregulation of protein turnover and autophagy has been implicated in its progression. Speckle-type POZ protein (SPOP), a substrate adaptor for the Cullin3-RING E3 ubiquitin ligase complex, plays an emerging role in protein homeostasis and transcriptional regulation. This study investigates the function of SPOP in cardiac hypertrophy and heart failure. RNA sequencing was performed to examine transcriptional changes in mouse hearts with cardiac-specific overexpression of SPOP, revealing differential expression of genes involved in autophagy, mitochondrial metabolism, and cardiac remodeling. These data provide new insights into the transcriptional landscape regulated by SPOP in the hypertrophic heart. Overall design: Cardiac-specific SPOP overexpression was generated using the aMHC-Cre system. Male mice aged 8–10 weeks were harvested for RNA extraction and sequencing. Total RNA was isolated using TRIzol, and libraries were prepared using poly(A) selection and sequenced on an Illumina platform. Differential gene expression analysis was conducted using DESeq2, and pathway enrichment was performed using GO and KEGG annotations. The dataset includes control (a-MHC-Cre) and SPOP overexpression(cKI) mice under sham conditions.