Cardiac troponin I (cTnI) is a key component of the Ca2+-regulatory mechanism of cardiac contractility. It is released into the circulation upon ischaemia and has become established as one of the principal diagnostic biomarkers of myocardial damage. The release of cTnI results in the generation of autoantibodies, and these have been suggested to play a pathogenic role. However, in this Edition of Clinical Science, Han, Y. et al. suggests that cTnI can act independently of immunological involvement, with the protein being found to increase infarct size caused by ischaemia/reperfusion (I/R) prior to the development of cTnI antibody. In vitro work shows that cTnI can induce increases in vascular cell adhesion molecule 1 (VCAM-1) expression and cell adhesion, with toll-like receptor 4 (TLR4) and nuclear factor kappa beta (NF-κB) involved in the downstream signalling.
Commentary| November 10 2016
Does extracellular cardiac troponin I play a pathogenic role independently of autoantibodies?
Charles S. Redwood
*Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, West Wing Level 6, John Radcliffe Hospital, Oxford OX3 9DU, U.K.
Correspondence: Charles S. Redwood (email email@example.com).
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Charles S. Redwood; Does extracellular cardiac troponin I play a pathogenic role independently of autoantibodies?. Clin Sci (Lond) 1 December 2016; 130 (24): 2277–2278. doi: https://doi.org/10.1042/CS20160493
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