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Related Experiment Video

Updated: Jul 15, 2026

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
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Transgenic MMP-2 expression induces latent cardiac mitochondrial dysfunction.

Hui-Zhong Zhou1, Xiaokui Ma, Mary O Gray

  • 1Cardiology Section, Department of Medicine, UCSF, VA Medical Center, 4150 Clement Street, 111C-5, San Francisco, CA 94121, USA.

Biochemical and Biophysical Research Communications
|May 4, 2007
PubMed
Summary

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Matrix metalloproteinases-2 (MMP-2) actively harms mitochondrial function during oxidative stress, abolishing cardioprotection. This finding reveals MMP-2 as a negative regulator, impacting heart injury recovery.

Area of Science:

  • Cardiovascular Biology
  • Mitochondrial Physiology
  • Protease Function

Background:

  • Matrix metalloproteinases (MMPs) are implicated in cardiac remodeling post-injury.
  • Dysfunctional ventricular remodeling contributes to heart failure progression.

Purpose of the Study:

  • To investigate the role of active matrix metalloproteinase-2 (MMP-2) in cardiac function and response to ischemia-reperfusion injury.
  • To determine if MMP-2 affects cardioprotection mediated by ischemic preconditioning (IPC).

Main Methods:

  • Utilized cardiac-specific transgenic mice expressing active MMP-2 (MMP-2 Tg).
  • Assessed cardiac phenotype, infarct size, and contractile performance after global ischemia-reperfusion.
  • Evaluated mitochondrial ultrastructure, respiration, lipid peroxidation, and cell necrosis in response to IPC.

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Published on: November 13, 2015

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Last Updated: Jul 15, 2026

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
09:16

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes

Published on: June 3, 2018

Improved Generation of Induced Cardiomyocytes Using a Polycistronic Construct Expressing Optimal Ratio of Gata4, Mef2c and Tbx5
10:05

Improved Generation of Induced Cardiomyocytes Using a Polycistronic Construct Expressing Optimal Ratio of Gata4, Mef2c and Tbx5

Published on: November 13, 2015

Main Results:

  • MMP-2 Tg hearts exhibited larger infarct sizes and impaired contractile function post-ischemia-reperfusion compared to wild-type.
  • Ischemic preconditioning (IPC) failed to provide cardioprotection in MMP-2 Tg hearts.
  • MMP-2 Tg hearts showed mitochondrial ultrastructural abnormalities, impaired respiration, increased lipid peroxidation, and cell necrosis.

Conclusions:

  • Active MMP-2 acts as a negative regulator of mitochondrial function during oxidative stress.
  • MMP-2 abolishes the protective effects of ischemic preconditioning.
  • Elevated MMP-2 activity exacerbates cardiac injury and impairs recovery after ischemic events.