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July 9, 2020CirculationOpen Access

FoxO1 binds to the promoters of 60% of cardiac-expressed genes at baseline and 91% after transverse aortic constriction, and its knockdown or deletion prevents endothelin-1- and pressure overload-induced cardiomyocyte hypertrophic growth.

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Why the study?

How transcription factors differentially regulate RNA polymerase II recruitment versus transcriptional elongation during cardiac hypertrophy remains unknown, and the scope of gene regulation by FoxO1 remains unexplored.

Population

Mouse hearts and in vitro cardiomyocytes

Comparison

Isoproterenol injections or transverse aortic constriction vs vehicle injection/sham surgery, and FoxO1 knockdown/deletion

Design

Preclinical animal and in vitro mechanistic study

Follow-up

7 days

Authors

JPJessica PflegerRCRyan C. ColemanJIJessica Ibetti

Discussion

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Overview

FoxO1 may coordinate pol II dynamics in hypertrophy; hypothesis-generating for transcription factor-targeted therapies in HF.

Structured PICO

P
Population
Mouse hearts subjected to 7 days of isoproterenol injections (3 mg·kg−1·mg−1) or transverse aortic constriction, and in vitro cardiomyocytes exposed to endothelin-1
I
Intervention
FoxO1 knockdown or deletion
C
Comparator
Vehicle injection or sham surgery
O
Outcome
FoxO1 chromatin binding, RNA polymerase II dynamics, gene expression, and cardiomyocyte hypertrophic growthsurrogate

FoxO1 mediates cardiac hypertrophic growth through extensive regulation of RNA polymerase II dynamics, highlighting its potential as a therapeutic target in cardiac hypertrophy.

Cite This Study

Pfleger et al. (2020) studied this question.

synapsesocial.com/papers/6a7ac2cabdf697b3de02c4e3https://doi.org/10.1161/circulationaha.120.046356
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1The Role and Molecular Mechanism of FoxO1 in Mediating Cardiac Hypertrophy2020 · 46 citations
  2. 2Forkhead box O6 (FoxO6) promotes cardiac pathological remodeling and dysfunction by activating Kif15–TGF‐β1 under aggravated afterload2023 · 8 citations
  3. 3FoxO1 is required for physiological cardiac hypertrophy induced by exercise but not by constitutively active PI3K2021 · 37 citations
  4. 4Targeting FoxO1 in Cardiovascular Diseases: Mechanisms and Therapeutic Potential2026 · 1 citations
  5. 5Abstract Wed035: Foxe1 Loss of Function Contributes to Adverse Remodeling in the Heart2025