Key result
Heart failure models downregulate metabolic genes via reduced PGC-1α occupancy and polymerase II recruitment.
Why the study?
It was unknown whether dysregulation of RNA polymerase II dynamics occurs in PGC-1α target genes in heart failure.
Population
Pressure-overload-induced heart failure mice, PGC-1α-cKO mice, and human failing hearts
Comparison
Pressure-overload-induced heart failure and PGC-1α knockout vs wild-type controls
Design
Preclinical animal and translational human tissue study
Authors
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Animal data implicate polymerase II dysregulation at PGC-1α targets in HF; leaves open human relevance and therapeutic translation.
Downregulation of metabolic genes in heart failure is partly driven by reduced PGC-1α occupancy and subsequent failure to recruit RNA polymerase II to target promoters.
Bhat et al. (2019) studied Heart failure. Pressure-overload and PGC-1α knockout vs. Wild-type mice under basal conditions was evaluated on Promoter occupancy of polymerase II and PGC-1α. In heart failure models, downregulation of PGC-1α target genes is attributed to reduced PGC-1α occupancy and polymerase II recruitment to metabolic gene promoters.
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