What type of study is this?

This is a Quantitative Study study.

October 9, 2025Circulation Research

Abstract Fri143: Constitutive Expression of Cardiomyocyte Klf9 Precipitates Metabolic Dysfunction and Spontaneous Heart Failure

Q: What is the clinical evidence from this study?

Study design: Other. Population: Heart failure. Intervention: Constitutive expression of Klf9 (Klf9KI) vs. Wt-Cre mice. Primary outcome: Cardiac hypertrophy, dysfunction, and failure.

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Key result

Cardiomyocyte Klf9 overexpression drives metabolic disruption, spontaneous hypertrophy, and heart failure by 8 weeks.

Population

Conditional Klf9 knock-in (Klf9KI) mice crossed with αMHC-Cre

Comparison

Constitutive expression of Klf9 vs Wt-Cre mice

Design

Preclinical

Follow-up

12-14 weeks

Authors

CTChandni ThakkarRutgers, The State University of New Jersey SASaleena AlikunjuUniversity of Miami AVAishwarya VenkatasubramanianRutgers, The State University of New Jersey

Discussion

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Implication

Constitutive expression of Klf9 in cardiomyocytes disrupts metabolic homeostasis, leading to progressive hypertrophy, heart failure, and early mortality in a mouse model.

Key Points

Klf9KI mice develop spontaneous heart failure indicated by a poor ejection fraction of 24% at 8 weeks, leading to early mortality.
Transcriptome analysis reveals significant changes in gene expression, particularly in metabolic genes, with 949 genes dysregulated by 4 weeks.
Mitochondrial function declines significantly by 4 weeks, correlating with a 3.5-fold increase in reactive oxygen species production.
Constitutive Klf9 expression disrupts metabolic homeostasis, highlighting its role in cardiac hypertrophy and dysfunction.

Structured PICO

Population

Conditional Klf9 knock-in mice evaluated up to 14 weeks of age to assess the impact of Klf9 overexpression on cardiac function and metabolism.

Intervention

Constitutive expression of Klf9 (3-4-fold increase in Klf9 expression)

Comparator

Wt-Cre mice

Outcome

Development of spontaneous hypertrophy, cardiac dysfunction, heart failure, and early mortality

Constitutive expression of Klf9 in cardiomyocytes disrupts metabolic homeostasis, leading to progressive hypertrophy, heart failure, and early mortality in a mouse model.

Cite This Study

Thakkar et al. (2025) studied Heart failure. Constitutive expression of Klf9 (Klf9KI) vs. Wt-Cre mice was evaluated on Cardiac hypertrophy, dysfunction, and failure. Constitutive expression of Klf9 in cardiomyocytes disrupts metabolic homeostasis, leading to spontaneous hypertrophy by 4 weeks, heart failure by 8 weeks, and early mortality by 12-14 weeks.

synapsesocial.com/papers/68e80eb363e2e2f707877d74 https://doi.org/10.1161/res.137.suppl_1.fri143

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Implication

Constitutive expression of Klf9 in cardiomyocytes disrupts metabolic homeostasis, leading to progressive hypertrophy, heart failure, and early mortality in a mouse model.

Abstract Fri143: Constitutive Expression of Cardiomyocyte Klf9 Precipitates Metabolic Dysfunction and Spontaneous Heart Failure

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Abstract Fri143: Constitutive Expression of Cardiomyocyte Klf9 Precipitates Metabolic Dysfunction and Spontaneous Heart Failure

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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