What is the clinical evidence from this study?

Study design: Other. Population: Cardiac hypertrophy. Intervention: Upf1 inactivation vs. Normal expression. Primary outcome: Cardiac hypertrophy and mRNA stability.

October 9, 2025Circulation Research

Abstract Wed015: Stress Induced RNA Decay In Cardiac Hypertrophy

View Full Paper

Ask AI

Bookmark

Key result

Upf1 loss drives cardiac hypertrophy and post-MI pathogenesis by altering mRNA stability via RBFox1.

Population

Cultured normal and hypertrophic cardiomyocytes, and mouse models of myocardial infarction

Comparison

Manipulation of Upf1 expression vs Control/normal conditions

Design

Preclinical

Authors

NSNingjing SongHubei University of Chinese Medicine SRSriram RavindranUniversity of North Carolina at Chapel Hill TLTian LiuShenyang Pharmaceutical University

Discussion

Member takes

Implication

Upf1 and RBFox1 regulate a novel NMD-independent mRNA decay pathway during cardiac hypertrophy, presenting a potential therapeutic target for cardiac remodeling.

Key Points

Altered mRNA stability was found in stressed myocytes, suggesting a new area of focus in cardiac hypertrophy.
Loss of Upf1 expression led to significant cardiac hypertrophy, highlighting its potential role in cellular homeostasis.
Using BRIC-Seq and other techniques, we uncovered the regulatory mechanisms of mRNA stability linked with Upf1.
Targeting Upf1-RBFox1 interactions may open new therapeutic avenues for managing cardiac diseases.

Structured PICO

Population

Cultured normal and hypertrophic cardiomyocytes, and mouse models of myocardial infarction

Intervention

Manipulation of Upf1 expression (loss of expression, restoring expression, AAV9 mediated Upf1 inactivation)

Comparator

Control/normal conditions

Outcome

Cardiac hypertrophy, mRNA stability, and cardiac pathogenesissurrogate

Upf1 and RBFox1 regulate a novel NMD-independent mRNA decay pathway during cardiac hypertrophy, presenting a potential therapeutic target for cardiac remodeling.

Cite This Study

Song et al. (2025) studied Cardiac hypertrophy. Upf1 inactivation vs. Normal expression was evaluated on Cardiac hypertrophy and mRNA stability. Loss of Upf1 expression led to cardiac hypertrophy and exacerbated myocardial infarction-induced pathogenesis, identifying a global shift of mRNA stability regulated by the Upf1-RBFox1 complex.

synapsesocial.com/papers/68e77f09d1c187e1c108fbed https://doi.org/10.1161/res.137.suppl_1.wed015

View Full Paper

Ask AI

Bookmark

Implication

Upf1 and RBFox1 regulate a novel NMD-independent mRNA decay pathway during cardiac hypertrophy, presenting a potential therapeutic target for cardiac remodeling.

Abstract Wed015: Stress Induced RNA Decay In Cardiac Hypertrophy

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Abstract Wed015: Stress Induced RNA Decay In Cardiac Hypertrophy

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Also Consider

Also Consider