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Cardiac troponin I and Cardiac Diseases

Troponin (Tn) is a regulatory protein related to myocardial and skeletal muscle contraction. It consists of three subunits: troponin I (TnI), troponin T (TnT) and troponin C (TnC). TnI can also be divided into three subtypes: skeletal muscle fast-response protein I (fsTnI), slow-reaction troponin I (ssTnI) and cardiac troponin I (cTnI).

Under normal circumstances, most cTnI combine with TnC to form a complex, and there are few free forms of cTnI in the cytoplasm. When the myocardium is complete, cTnI cannot enter the blood circulation through the cardiac membrane. Therefore, it is difficult to detect cTnI in plasma under normal conditions. When myocardial degeneration and necrosis occur due to ischemia and hypoxia, cTnI can enter the interstitium through the damaged myocardial membrane and then enter the blood vessels and lymphatic vessels. Plasma cTnI can be increased to 5-50 times of normal people within 3-12 hours of myocardial injury, which can last for a week or more. The plasma cTnI of patients with myocardial infarction began to increase at the early stage, and increased significantly after 4h, reaching the peak at 18h, averaging 112pg/L, and the abnormal increase lasted 6 to 8 days. The specificity of cTnI in diagnosing myocardial infarction is 96%, and its sensitivity is 97%, and it can effectively distinguish skeletal muscle from other tissue injuries, which is more sensitive and specific than lactate dehydrogenase, creatine kinase and other indicators.

Hypertensive myocardial hypertrophy is an autosomal dominant hereditary disease associated with ventricular hypertrophy and muscle fiber disorder, and is the most common cause of sudden death in young people. Kimura et al. systematically studied the submyogenes of 184 patients with cardiac hypertrophy, including cTnI, actin and cTnC, and found that many patients had mutations in cTnI genes. Family analysis also found that the 145th Arg mutation in cTnI protein was Gly, or the 206th Lys mutation was Gly, suggesting that cTnI mutation may be one of the causes of cardiac hypertrophy.

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