Chronic AMD3100 antagonism of SDF-1α–CXCR4 exacerbates cardiac dysfunction and remodeling after myocardial infarction

Increasing cardiac contractility after myocardial infarction exacerbates cardiac injury and pump dysfunction.

RATIONALE Myocardial infarction (MI) leads to heart failure (HF) and premature death. The respective roles of myocyte death and depressed myocyte contractility in the induction of HF after MI have not been clearly defined and are the focus of this study. OBJECTIVES We developed a mouse model in which we could prevent depressed myocyte contractility after MI and used it to test the idea that p...

Integrative Physiology Increasing Cardiac Contractility After Myocardial Infarction Exacerbates Cardiac Injury and Pump Dysfunction

Increased C-reactive protein expression exacerbates left ventricular dysfunction and remodeling after myocardial infarction.

We previously reported serum C-reactive protein (CRP) elevation after acute myocardial infarction (MI) to be associated with adverse outcomes including cardiac rupture, left ventricular (LV) remodeling, and cardiac death. Experimental studies have indicated that CRP per se has various biological actions including proinflammatory and proapoptotic effects, suggesting a pathogenic role of CRP in t...

Inhibition of TGF-beta signaling exacerbates early cardiac dysfunction but prevents late remodeling after infarction.

OBJECTIVE Transforming growth factor (TGF)-beta promotes the deposition of extracellular matrix protein and also acts as an anti-inflammatory cytokine. These biological effects might be involved in the development and progression of left ventricular (LV) remodeling and failure after myocardial infarction (MI). However, its pathophysiological significance remains obscure in post-MI hearts. MET...

Transient receptor potential vanilloid gene deletion exacerbates inflammation and atypical cardiac remodeling after myocardial infarction.

The transient receptor potential vanilloid (TRPV1) channels expressed in sensory afferent fibers innervating the heart may be activated by protons or endovanilloids released during myocardial ischemia (MI), leading to angina. Although our previous in vitro data indicate that TRPV1 activation may preserve cardiac function after ischemia-reperfusion injury, the underlying mechanisms are largely u...