Pressure Overload Model
Objective: To assess myocardial adaptive responses to pressure overload by inducing cardiac hypertrophy and fibrosis through moderate or high-intensity pressure overload in mice, with focus on the role of cardiac fibroblasts and KLF5 in these responses
This is a Pressure Overload Model protocol using mouse as the model organism. The procedure involves 4 procedural steps, 1 materials. Extracted from a 2009 paper published in Journal of Clinical Investigation.
Model and subjects
mouse • Not specified in provided text • unknown • Not specified in provided text • Not specified in provided text
Study window
Estimated timing pending
Core workflow
Induce moderate-intensity pressure overload • Induce high-intensity pressure overload • Assess cardiac fibroblast-specific Klf5 deletion effects
Primary readouts
- Cardiac fibrosis development
- Cardiac hypertrophy response
- Heart failure severity
- Survival/mortality
Key equipment and reagents
Verified items
0
Direct vendor links
0
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Protocol Steps
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Induce moderate-intensity pressure overload
Apply moderate-intensity pressure overload to induce cardiac fibrosis and hypertrophy in mice
Note: Moderate-intensity pressure overload suppressed cardiac fibrosis and hypertrophy in Klf5 haploinsufficient mice but not in cardiomyocyte-specific Klf5 deletion mice
View evidence from paper
“Haploinsufficiency of the transcription factor-encoding gene Krüppel-like factor 5 (Klf5) suppressed cardiac fibrosis and hypertrophy elicited by moderate-intensity pressure overload”
Induce high-intensity pressure overload
Apply high-intensity pressure overload to assess severe cardiac responses and heart failure development
Note: High-intensity pressure overload caused severe heart failure and early death in mice with Klf5-null fibroblasts
View evidence from paper
“High-intensity pressure overload caused severe heart failure and early death in mice with Klf5-null fibroblasts”
Assess cardiac fibroblast-specific Klf5 deletion effects
Evaluate cardiac hypertrophy and fibrosis responses in mice with cardiac fibroblast-specific Klf5 deletion
Note: Cardiac fibroblast-specific Klf5 deletion ameliorated both cardiac hypertrophy and fibrosis, indicating KLF5 in fibroblasts is important for pressure overload response
View evidence from paper
“cardiac fibroblast-specific Klf5 deletion ameliorated cardiac hypertrophy and fibrosis, indicating that KLF5 in fibroblasts is important for the response to pressure overload”
Administer IGF-1 peptide inhibitor during high-intensity pressure overload
Administer peptide inhibitor of IGF-1 to mice undergoing high-intensity pressure overload to assess IGF-1's role in cardioprotection
Note: IGF-1 inhibition severely exacerbated heart failure, demonstrating IGF-1 induction is essential for cardioprotective responses
View evidence from paper
“administration of a peptide inhibitor of IGF-1 severely exacerbated heart failure induced by high-intensity pressure overload”