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May 1, 2021The FASEB Journal

Ang 1-7 treatment attenuated the development of HFD + L-NAME-induced HFpEF, reduced cardiac hypertrophy, and improved metabolic function, associated with reduced STAT3 and increased AMPK expression.

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Why the study?

Existing renin-angiotensin system inhibitors provide modest to negligible benefits in HFpEF, motivating evaluation of the therapeutic role and molecular mechanisms of Ang 1-7.

Does Angiotensin 1-7 improve diastolic dysfunction and cardiac hypertrophy in a murine model of HFpEF?

Population

Male WT mice subjected to HFD and L-NAME

Comparison

Ang 1-7 (24 ug/kg/day) vs saline

Design

Preclinical animal study

Follow-up

4 weeks

Authors

PEPariya EdalatKGKarina Pereira GomesNBNoura Ballasy

Discussion

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Member takes

Overview

ACE2 modulation may extend RAS targeting in HFpEF models; leaves open clinical translation and efficacy in humans.

Structured PICO

Does Angiotensin 1-7 improve diastolic dysfunction and cardiac hypertrophy in a murine model of HFpEF?

P
Population
Male WT mice subjected to high-fat diet (HFD) and eNOS inhibition with L-NAME (0.5 g/L in drinking water) to generate a murine model of HFpEF
I
Intervention
Angiotensin 1-7 (24 ug/kg/day) for 4 weeks
C
Comparator
Saline for 4 weeks
O
Outcome
Development of diastolic dysfunction and cardiac hypertrophysurrogate

In a murine model of HFpEF, Angiotensin 1-7 attenuated diastolic dysfunction and cardiac hypertrophy, suggesting a potential therapeutic role.

Cite This Study

Edalat et al. (2021) studied this question.

synapsesocial.com/papers/6a6fd7c826770c2b8de03142https://doi.org/10.1096/fasebj.2021.35.s1.00406
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