Cardiac troponins: Mechanisms of release and role in healthy and diseased subjects

Abstract

The cardiac troponins (cTns), cardiac troponin C (cTnC), cTnT, and cTnI are key elements of myocardial apparatus, fixed as protein complex on the thin filament of sarcomere and are involved in the regulation of excitationcontraction coupling of cardiomyocytes in the presence of Ca 2+ . Circulating cTnT and cTnI (cTns) increase following cardiac tissue necrosis, and they are consolidated biomarkers of acute myocardial infarction (AMI). However, the use of high sensitivity (hs)-immunoassay tests for cTnT and cTnI has made it possible to identify a multitude of other clinical conditions associated with increased circulating levels of cTns. cTns can be measured also in the peripheral circulation of healthy subjects or athletes, suggesting that different mechanisms are involved in the release of cTns in the blood independently of cardiac cell necrosis. In this review, the molecular/cellular mechanisms involved in cTns release in blood and the exploitation of cTnI and cTnT as biomarkers of cardiac adverse events, in addition to cardiac necrosis, are discussed.

Left ventricular remodeling and its correlation with serum cardiac troponin I in patients with end-stage renal disease treated

“…34 A sustained increase in cTnI of less than 20% is considered characteristic of chronic myocardial injury, such as chronic kidney disease, diabetes, significant left ventricular hypertrophy, chronic heart failure and other diseases resulting in secondary chronic myocardial injury. 35 Although renal function can affect the clarity of cTnI, the main mechanism of its elevation is still caused by myocardial injury. 36 Domestic research shows that the serum cTnT level is positively correlated with LVMI.…”

Use of Cardiac Troponin for the Diagnosis of Cardiac Pathology in Postmortem Samples Taken at Autopsy

“…Initially, it was thought that cTn could only be released following overt cellular necrosis; however, recently it has been suggested that release can occur in ischemia without necrosis [3]. A review of the subject by Ragusa and colleagues suggest release mechanisms, including apoptosis, necroptosis, physiological cardiomyocyte renewal, and cellular wounding can contribute to cTn release as well as necrosis [4]. An immunohistochemical study using a canine model of coronary occlusion ranging from 30 minutes to 6 hours demonstrated variable loss of both cTnT and cTnI in paraffin-embedded left ventricular myocardial sections [5].…”