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December 12, 2018HypertensionOpen Access

Mice with myeloid cell-restricted MR deficiency or those receiving targeted MR antagonists showed improved cardiac function, enhanced infarct neovascularization, and scar maturation compared to WT controls.

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Why the study?

Does targeted macrophage mineralocorticoid receptor antagonism improve cardiac wound repair and remodeling in mice after myocardial infarction?

Population

Mice subjected to left coronary artery ligation

Comparison

Myeloid cell-restricted MR deficiency vs WT controls

Design

Animal study

Authors

DFDaniela FraccarolloSTSvenja ThomasCSClaus Jürgen Scholz

Discussion

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Member takes

Overview

Macrophage-targeted MR antagonism merits further preclinical testing post-MI; leaves open any role in human remodeling or therapy.

Key Points

  • The study aims to determine the role of the macrophage mineralocorticoid receptor in cardiac wound healing following myocardial infarction.
  • Used myeloid cell-restricted MR-deficient mice and wild type controls post-left coronary artery ligation for assessment of cardiac function and remodeling.
  • Analyzed gene expression profiles of macrophages in the ischemic heart to determine differentiation and healing factors.
  • Evaluated the effects of MR antagonists delivered to macrophages during myocardial infarction.
  • Cardiac function and remodeling improved in MR-deficient mice compared to wild type controls with enhanced infarct neovascularization and scar maturation.
  • MR deletion altered macrophage phenotype, affecting wound healing factors beyond the M1/M2 model.
  • Single administration of MR antagonists led to better healing response and reduced cardiac remodeling.

Structured PICO

Does targeted macrophage mineralocorticoid receptor antagonism improve cardiac wound repair and remodeling in mice after myocardial infarction?

P
Population
Mice subjected to left coronary artery ligation (myocardial infarction model), including myeloid cell-restricted mineralocorticoid receptor (MR) deficient mice and wild type (WT) controls.
I
Intervention
Genetic myeloid cell-restricted mineralocorticoid receptor (MR) deficiency, or targeted delivery of MR antagonists (RU28318 or eplerenone-containing liposomes) to macrophages via a single administration at the onset of myocardial infarction.
C
Comparator
Wild type (WT) controls.
O
Outcome
Cardiac function and remodeling, infarct neovascularization, and scar maturation evaluated 7 days after left coronary artery ligation.surrogate

Targeted delivery of mineralocorticoid receptor antagonists to macrophages improves myocardial infarct healing and protects against adverse cardiac remodeling in a preclinical mouse model.

Cite This Study

Fraccarollo et al. (2018) studied this question.

synapsesocial.com/papers/6a23866cb7e293e61ca5e860https://doi.org/10.1161/hypertensionaha.118.12162
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