Author + information
- Richard L. Popp, MD∗ ()
- ↵∗Stanford University School of Medicine, Cardiovascular Medicine, Biodesign Program, Room E-100-D, The James H. Clark Center, 318 Campus Drive West, Stanford, California 94305
The letter from Dr. Peng and colleagues calls attention to their previous article reporting a graded protective effect of cardiac troponin (cTn) at high concentrations on isolated neonatal rat myocardial cells subjected to hypoxia. This suggests that cTn may be an “actor” at the time of acute myocellular injury, with a beneficial effect, and not simply a “messenger” of the acute damage. They endorse the premise that cTn may have a role in later, or ongoing, myocardial injury (1). Heat shock protein-60 apparently has a “good” influence in an acute situation and a “bad” effect via autoimmune mechanisms in the long term (2). This example may be another cogent analogy to the mechanism that I proposed for cTn.
I appreciate both their comments and their participation in what hopefully will be an ongoing investigation by many in the research community. We need to better understand the possible role of cTn and other proteins related to myocardial injury in the currently opaque path leading from initial myocardial insult to cardiac dysfunction months to years later.
Please note: Dr. Popp is a paid consultant to Singulex Corporation, which makes immunoassay equipment for measurement of the biomarkers discussed in the viewpoint; he holds no equity in the company.
- American College of Cardiology Foundation