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May 18, 2015OncotargetOpen Access

Combined effects of aging and inflammation on renin-angiotensin system mediate mitochondrial dysfunction and phenotypic changes in cardiomyopathies

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Why the study?

Does losartan improve cardiac mitochondrial dysfunction and phenotypic changes in mouse models of aging and inflammation?

Population

Male C57BL/6J wild-type (WT) and IL-10 knockout (IL-10−/−) mice, young (4–6 months) and aged (22–24 months)

Comparison

Losartan ad libitum in drinking water for 4 weeks vs Placebo (untreated) age- and genotype-matched mice

Design

Preclinical

Follow-up

4 weeks

Authors

TBTyesha N. BurksRMRuth MarxLPLaura Powell

Discussion

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Overview

Losartan effects on cardiac remodeling merit human trials in inflammatory cardiomyopathy; leaves open mitochondrial benefits and clinical translation.

Structured PICO

Does losartan improve cardiac mitochondrial dysfunction and phenotypic changes in mouse models of aging and inflammation?

P
Population
Male C57BL/6J wild-type (WT) and IL-10 knockout (IL-10−/−) mice, young (4–6 months) and aged (22–24 months)
I
Intervention
Losartan (0.6 g/L for young mice and 0.9 g/L for aged mice) ad libitum in drinking water for 4 weeks
C
Comparator
Placebo (untreated) age- and genotype-matched mice
O
Outcome
Expression of localized cardiac angiotensin II type I and type II receptors (AT1R, AT2R), downstream effectors (Nox2, Nox4), mitochondrial function, and phenotypic outcomes (hypertrophy, fibrosis)surrogate

In a mouse model, the combination of aging and inflammation causes distinct molecular changes in the cardiac renin-angiotensin system that lead to cardiomyopathy, which can be partially reversed by AT1R blockade with losartan.

Cite This Study

Burks et al. (2015) studied this question.

synapsesocial.com/papers/6a0a51eedf43cb70ca574181https://doi.org/10.18632/oncotarget.3979
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Also Consider

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