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August 23, 2026Japanese Circulation Journal-english Edition

Anti-MCP-1 gene therapy reduces 4-week mortality ~67% and attenuates LV remodeling in mice with MI.

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Why the study?

Increased MCP-1 expression has been described in failing hearts, but its pathophysiological significance in heart failure remains obscure.

Does anti-MCP-1 gene therapy improve survival and attenuate left ventricular remodeling in mice after experimental myocardial infarction?

Population

Mice with anterior MI induced by left coronary artery ligation

Comparison

Transfection with N-terminal deletion mutant of human MCP-1 gene vs nontreated MI

Design

Experimental animal study

Follow-up

4 weeks

Key result

Anti-MCP-1 gene therapy improved the 4-week survival rate in mice with myocardial infarction compared to no treatment (87% vs 61%, P<0.05) and attenuated left ventricular remodeling.

Authors

SHShunji HayashidaniHTHiroyuki TsutsuiTSTetsuya Shiomi

Discussion

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Overview

MCP-1 blockade attenuates post-MI remodeling in mice; leaves open therapeutic relevance in human HF.

Key Points

  • To determine whether monocyte chemoattractant protein-1 (MCP-1) is elevated after myocardial infarction and if its blockade can mitigate left ventricular remodeling and failure.
  • Induced anterior myocardial infarction in mice by ligating the left coronary artery.
  • Transfected an N-terminal deletion mutant of the human MCP-1 gene into skeletal muscle 3 days before and 14 days after ligation to inhibit MCP-1 signaling.
  • Assessed left ventricular function, remodeling, survival, macrophage infiltration, and cytokine expression over a 4-week follow-up period.
  • Myocardial MCP-1 mRNA expression increased 40-fold in the noninfarcted left ventricle at 1 day post-infarction and remained elevated for 28 days.
  • Anti-MCP-1 gene therapy significantly improved 4-week post-infarction survival compared with untreated controls (87% vs. 61%, P<0.05).
  • Therapy attenuated left ventricular cavity dilatation, contractile dysfunction, interstitial fibrosis, macrophage recruitment, and expression of TNF-alpha and TGF-beta despite comparable infarct size.

Structured PICO

Does anti-MCP-1 gene therapy improve survival and attenuate left ventricular remodeling in mice after experimental myocardial infarction?

P
Population
Mice with experimentally induced anterior myocardial infarction followed for 4 weeks.
I
Intervention
N-terminal deletion mutant of the human MCP-1 gene transfected into limb skeletal muscle 3 days before and 14 days after ligation
C
Comparator
Nontreated MI mice
O
Outcome
Survival rate at 4 weeks and left ventricular remodeling (cavity dilatation, contractile dysfunction, interstitial fibrosis)surrogate

Main Result

Absolute Event Rate: 87% vs 61%

p-value: p=<0.05

Anti-MCP-1 gene therapy improves survival and attenuates adverse left ventricular remodeling in a murine model of myocardial infarction, suggesting a potential novel strategy for preventing post-MI heart failure.

Cite This Study

Hayashidani et al. (2003) studied Myocardial Infarction. Anti-MCP-1 gene therapy vs. Nontreated MI mice was evaluated on Survival rate at 4 weeks (p=<0.05). Anti-MCP-1 gene therapy improved the 4-week survival rate in mice with myocardial infarction compared to no treatment (87% vs 61%, P<0.05) and attenuated left ventricular remodeling.

synapsesocial.com/papers/6a8a66a35416a23081b2e36bhttps://doi.org/10.1161/01.cir.0000092890.29552.22
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