What is the clinical evidence from this study?

Population: Myocardial infarction. Intervention: Cardiac MCP-1 overexpression. Primary outcome: Left ventricular (LV) dysfunction and remodeling.

What question did this study set out to answer?

To investigate the effect of cardiac-specific monocyte chemoattractant protein-1 (MCP-1) overexpression on left ventricular dysfunction and remodeling following myocardial infarction.

September 22, 2006Circulation ResearchOpen Access

Cardiac Overexpression of Monocyte Chemoattractant Protein-1 in Transgenic Mice Prevents Cardiac Dysfunction and Remodeling After Myocardial Infarction

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Key result

Cardiac overexpression of MCP-1 in transgenic mice reduced infarct area and scar formation, and prevented LV dysfunction and remodeling after myocardial infarction.

Why the study?

Does cardiac overexpression of MCP-1 prevent LV dysfunction and remodeling after myocardial infarction in a murine model?

Key Points

To investigate the effect of cardiac-specific monocyte chemoattractant protein-1 (MCP-1) overexpression on left ventricular dysfunction and remodeling following myocardial infarction.
Generated alpha-cardiac myosin heavy chain promoter-driven MCP-1 transgenic mice (MHC/MCP-1) and subjected them to experimental myocardial infarction.
Evaluated infarct size, left ventricular function, macrophage recruitment, neovascularization, endothelial progenitor cell mobilization, and Tie2/LacZ bone marrow chimera engraftment.
Performed in vitro cardiomyocyte and cardiac fibroblast assays to evaluate IL-6 synergistic STAT3 activation and myofibroblast differentiation under hypoxic conditions.
MHC/MCP-1 mice exhibited reduced infarct size, attenuated scar formation, and preserved left ventricular function after myocardial infarction.
Transgenic hearts showed elevated macrophage infiltration, accelerated neovascularization, heightened IL-6 secretion, pronounced STAT3 activation, and cardiac myofibroblast accumulation.
In vitro analyses demonstrated that MCP-1 synergized with IL-6 to sustain STAT3 activation in cardiomyocytes and directly drove fibroblast-to-myofibroblast differentiation alongside hypoxia.

Structured PICO

Does cardiac overexpression of MCP-1 prevent LV dysfunction and remodeling after myocardial infarction in a murine model?

Population

Murine myocardial infarction (MI) model using transgenic mice expressing the mouse JE-MCP-1 gene under the control of the alpha-cardiac myosin heavy chain promoter (MHC/MCP-1 mice)

Intervention

Cardiac overexpression of monocyte chemoattractant protein-1 (MCP-1)

Comparator

Control mice (implied)

Outcome

Left ventricular (LV) dysfunction and remodeling after myocardial infarctionsurrogate

Cardiac overexpression of MCP-1 prevents LV dysfunction and remodeling after myocardial infarction in mice by inducing macrophage infiltration, neovascularization, and myofibroblast accumulation.

Discussion

No takes yet. Share an insight, caveat, or question.

Implication

Should not change post-MI care; hypothesis-generating for MCP-1 in remodeling.

Cite This Study

Morimoto et al. (2006) studied Myocardial infarction. Cardiac MCP-1 overexpression was evaluated on Left ventricular (LV) dysfunction and remodeling. Cardiac overexpression of MCP-1 in transgenic mice reduced infarct area and scar formation, and prevented LV dysfunction and remodeling after myocardial infarction.

synapsesocial.com/papers/6a0efa2406ecbe83344805eb https://doi.org/10.1161/01.res.0000246113.82111.2d

Topics

Echocardiography

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Cardiac Overexpression of Monocyte Chemoattractant Protein-1 in Transgenic Mice Prevents Cardiac Dysfunction and Remodeling After Myocardial Infarction

Key Points

Structured PICO

Discussion

Implication

Cite This Study

Topics

Cardiac Overexpression of Monocyte Chemoattractant Protein-1 in Transgenic Mice Prevents Cardiac Dysfunction and Remodeling After Myocardial Infarction

Key Points

Structured PICO

Discussion

Implication

Cite This Study

Also Consider

Topics

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