Myocardial remodeling after infarction: the role of myofibroblasts.

Myofibroblasts have characteristics of fibroblasts and smooth muscle cells: they produce extracellular matrix and are able to contract. In so doing, they can contribute to tissue replacement and interstitial fibrosis following cardiac injury. The scar formed after myocardial injury is no longer considered to be passive tissue; it is an active playground where myofibroblasts play a role in collagen turnover and scar contraction.

Mouse strain determines the outcome of wound healing after myocardial infarction.

Aims: Our objective was to study the effect of the genetic background on the wound healing process after myocardial infarction (MI) in mice.

Methods And Results: MI was induced in five different mouse strains (BalbC, C57Bl6, FVB, 129S6, and Swiss). At 3, 14, and 28 days after MI, cardiac dimensions were monitored by echocardiography and histology, whereas cardiac function was determined by direct intraventricular pressure measurements (dP/dt).

Molecular imaging for efficacy of pharmacologic intervention in myocardial remodeling.

Objectives: Using molecular imaging techniques, we examined interstitial alterations during postmyocardial infarction (MI) remodeling and assessed the efficacy of antiangiotensin and antimineralocorticoid intervention, alone and in combination.

Background: The antagonists of the renin-angiotensin-aldosterone axis restrict myocardial fibrosis and cardiac remodeling after MI and contribute to improved survival. Radionuclide imaging with technetium-99m-labeled Cy5.

Molecular imaging of interstitial alterations in remodeling myocardium after myocardial infarction.

Objectives: The purpose of this study was to evaluate interstitial alterations in myocardial remodeling using a radiolabeled Cy5.5-RGD imaging peptide (CRIP) that targets myofibroblasts.

Background: Collagen deposition and interstitial fibrosis contribute to cardiac remodeling and heart failure after myocardial infarction (MI).

Defective intercellular adhesion complex in myocardium predisposes to infarct rupture in humans.

Objectives: Our goal was to evaluate intercellular adhesion complex proteins in myocardium in human infarct rupture.

Background: Infarct rupture, a fatal complication of myocardial infarction (MI), has been attributed to a defective cell adhesion complex in a transgenic mouse model.

Methods: Heart samples were collected from autopsies from infarct rupture and control (nonrupture) MI patients.

Increased matrix metalloproteinase-8 and -9 activity in patients with infarct rupture after myocardial infarction.

Background: Infarct rupture is a usually fatal complication of myocardial infarction (MI), for which no molecular mechanism has been described in humans. Experimental evidence in mouse models suggests that the degradation of the extracellular matrix by matrix metalloproteinases (MMPs) plays an important role in infarct rupture. The present study was designed to study the role of MMP-2, MMP-8, and MMP-9 in human infarct rupture.

Interruption of Wnt signaling attenuates the onset of pressure overload-induced cardiac hypertrophy.

The hypertrophic response of the heart has been recognized recently as the net result of activation of prohypertrophic and antihypertrophic pathways. Here we report the involvement of the Wnt/Frizzled pathway in the onset of cardiac hypertrophy development. Stimulation of the Wnt/Frizzled pathway activates the disheveled (Dvl) protein.