Cellular & Molecular Interactions in cardiac inflammation
Cellular & Molecular Interactions in cardiac inflammation may give rise to potential combination therapies.
The major cause of acute myocardial infarction (MI) is the complete or partial occlusion of one or more of the major coronary arteries resulting in inadequate blood flow to cardiac muscle tissue. When coronary artery occlusion occurs, the resulting ischemia causes decreased availability of free energy from ATP and failure of ion channel function, which in turn induces cardiomyocyte death. Although rapid reperfusion of the ischemic area is the most effective means of rescuing myocardial tissue, significant changes take place at the level of the tissues, cells, and molecules within the heart even despite reperfusion therapy
This eBook is an overview of the inflammatory events at the tissue, cellular and molecular levels following post-MI:
Overview of preclinical models and their advantages/disadvantages
Cellular and molecular interactions
Review of some of the current therapies and new research focus
Recent research has focused on opportunities to provide pharmaceutical cardioprotection by targeting the inflammatory cascade in the hope of steering it toward resolution, repair, and recovery and away from tissue damage, excessive fibrosis, and dysfunction. This eBook is meant to provide an overview of potential targeted molecular intervention therapies
Excerpt from the eBook:
"A broad range of complex endocrine, paracrine, and autocrine signaling in post-ischemic myocardium offers many opportunities for pharmacological manipulation of the inflammatory microenvironment to promote resolution, repair, and recovery and prevent further damage, excessive scarring, and dysfunction that may lead to life-threatening complications."