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Related Experiment Video

Updated: Jul 23, 2025

A Murine Closed-chest Model of Myocardial Ischemia and Reperfusion

A Murine Closed-chest Model of Myocardial Ischemia and Reperfusion

Published on: July 17, 2012

Brown Adipose Tissue and BMP3b Decrease Injury in Cardiac Ischemia-Reperfusion.

Íngrid Martí-Pàmies¹, Robrecht Thoonen^1,2, Michael Morley¹

¹Cardiovascular Institute, Perelman School of Medicine at the University of Pennsylvania, Philadelphia (I.M.-P., M.M., L.G., J.T., A.C., K.M., L.L., M.S.-C.).

Circulation Research

|July 18, 2023

Summary

This summary is machine-generated.

Brown adipose tissue (BAT) protects the heart from ischemia-reperfusion (I/R) injury. The study identified bone morphogenetic protein 3b (BMP3b) secreted by BAT as a key factor in this cardioprotective effect, offering new therapeutic targets.

Keywords:

heart failure mice myocardium reperfusion uncoupling protein 1

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Last Updated: Jul 23, 2025

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Area of Science:

Cardiology
Metabolism
Molecular Biology

Background:

Myocardial infarction (MI) remains a major cause of heart failure and death globally.
Ischemia-reperfusion (I/R) injury significantly contributes to cardiac damage post-MI.
Brown adipose tissue (BAT) activation has been observed in MI, with secreted factors potentially impacting cardiac health.

Purpose of the Study:

To investigate the protective role of BAT against cardiac injury in I/R settings.
To identify specific cardioprotective proteins secreted by BAT.
To elucidate the therapeutic potential of BAT-derived factors in mitigating I/R-induced myocardial damage.

Main Methods:

Utilized wild-type (WT) and uncoupling protein 1 (Ucp1)-deficient mice for I/R surgery, with and without BAT transplantation.
Employed RNA sequencing (RNA-seq) to identify potential cardioprotective factors secreted by BAT.
Investigated the role of bone morphogenetic protein 3b (BMP3b) by using deficient mice and direct BMP3b treatment.

Main Results:

Impaired BAT function exacerbated I/R-induced MI size, while BAT transplantation reduced it.
BMP3b was identified as a BAT-secreted protein that attenuated I/R injury in mice.
BMP3b treatment decreased MI size, mediated via SMAD1/5/8 signaling, and elevated plasma BMP3b levels correlated with cardiac injury in humans.

Conclusions:

BAT and its secreted protein BMP3b play a significant cardioprotective role in I/R injury.
Targeting BMP3b or SMAD1/5 signaling presents a promising therapeutic strategy for reducing myocardial damage.
This research highlights a novel link between metabolic tissue and cardiac protection.