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January 24, 2005European Heart JournalOpen Access

Myocardial infarction increases ACE2 expression in rat and humans

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Why the study?

Does myocardial infarction and subsequent ramipril treatment alter the expression of ACE2 in rats and human failing hearts?

Population

Rats with myocardial infarction and human failing hearts

Comparison

Ramipril (1 mg/kg) for 4 weeks (in rats) vs Control rats and viable myocardium

Design

Preclinical

Follow-up

Up to 28 days (4 weeks)

Authors

LBLouise M. BurrellHeart Failure & TransplantJRJohn RisvanisThe University of MelbourneEKEiji KubotaNagoya City University

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Implication

MI-induced ACE2 upregulation persists despite ramipril in rats; leaves open compensatory RAS role in human post-MI remodeling.

Key Points

  • This research aims to understand how myocardial infarction affects ACE2 expression in both rats and human hearts.
  • Rats were assessed at days 1, 3, and 28 post-myocardial infarction.
  • Ramipril was administered for 4 weeks to evaluate its effects on cardiac ACE2 expression.
  • ACE and ACE2 gene expression were analyzed using quantitative real-time PCR and immunohistochemistry.
  • Both ACE and ACE2 mRNA increased significantly in the myocardial infarct area by day 3 (ACE P=0.022, ACE2 P=0.015).
  • At day 28, elevated ACE (P=0.005) and ACE2 (P=0.006) mRNA levels were found in viable myocardium of MI rats compared to controls.
  • In humans with heart failure, increased immunoreactivity for ACE and ACE2 was observed.

Structured PICO

Does myocardial infarction and subsequent ramipril treatment alter the expression of ACE2 in rats and human failing hearts?

P
Population
Rats with myocardial infarction and human failing hearts
I
Intervention
Ramipril (1 mg/kg) for 4 weeks (in rats)
C
Comparator
Control rats and viable myocardium
O
Outcome
Cardiac gene and protein expression of ACE and ACE2surrogate

Myocardial infarction increases ACE2 expression in both rat models and human failing hearts, which is not attenuated by ACE inhibition, suggesting a compensatory role in the renin-angiotensin system.

Cite This Study

Burrell et al. (2005) studied this question.

synapsesocial.com/papers/6a1beff44ebd09f3dfa93aafhttps://doi.org/10.1093/eurheartj/ehi114
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