What is cardiac troponin

A healthy heart can guarantee the health of your body, so now many people pay special attention to the health of their heart in order to ensure their own health. So they want to have a comprehensive understanding of what cardiac troponin is? In order for you to have a comprehensive understanding, please take a look at the detailed introduction below. I believe that through this introduction you can have a comprehensive understanding.

Troponin T (TnT) has a molecular weight of 37KD and is the tropomyosin binding subunit. There are three isoforms: skeletal muscle troponin T (sTnT) includes fast skeletal muscle type and slow skeletal muscle type, in addition to cardiac muscle type. Most of cardiac troponin T (cTnT) exists in the form of CTI complexes on the filaments, and 6%-8% exists in the free form in the myocardial cytoplasm. Because the genes encoding cTnT and skeletal muscle TnT are different, cTnT is not expressed in skeletal muscle. cTnT was 40% heterologous to the two skeletal muscle isoforms. The cTnT molecule is stable, hydrophilic, and has good reactivity with specific antigenic determinants. The monoclonal antibodies currently used are capture antibodies and labeling antibodies specific to the myocardium.

There are three subtypes of TnI (troponin I): skeletal muscle troponin I (sTnI) has fast skeletal muscle type and slow skeletal muscle type, which have similar molecular weight (20KD), but there is about 40% difference in amino acid sequence between the two; the third is the myocardial type. There is also a 40% difference in the amino acid sequence between cardiac troponin I (cTnI) and the skeletal muscle type. However, the amino terminus of human eTnI has 31 more amino acids than sTnI, making its molecular weight reach 22KD. This unique sequence gives it a high myocardial specificity and helps to prepare the corresponding monoclonal antibody. cTn exists in myocardial cells in the form of cTnI-CT complex and free cTnI. After being released into the blood circulation when the myocardium is damaged, cTnI-CT can be further decomposed into cTnI-C complex and free cTnI. Therefore, in addition to cTnI CT and free cTnI, there is also cTnI-C in the blood circulation, and cTnI-C is its main form in the blood. Its metabolites are excreted from the body by the kidneys.

TnC has a molecular weight of 18KD and is a Ca binding subunit, with each molecule binding 2 Ca. The structure of TnC in cardiac and skeletal muscle is the same.

Since cTnT and cTnI are encoded by different genes and have different amino acid sequences and unique antigenicity from their heterozygous forms in skeletal muscle, their specificity is significantly better than that of CK-MB isoenzymes. When muscle tissue other than the myocardium is damaged or diseased, CK and CK-MB may increase, while cTnT and cTnI will not exceed their critical values. Because their contents in normal serum are extremely low, they increase significantly during AMI, and the increase is generally greater than the changes in total CK and CK-MB. Due to their small molecular weight, cTnT and cTnI are rapidly released from the myocardial cell plasma into the blood after the onset of the disease, and their concentration in the blood increases rapidly, with the time being equivalent to or slightly earlier than that of CK-MB. Although the half-life of troponin is very short (cTnT 2 hours, the half-life of free cTnI is reported to vary from 2h to 5d), its degradation process from myofibrils lasts a long time and can remain elevated in the blood for a long time. Therefore, it has the advantages of early increase of CK-MB and long diagnostic time window of LD1. Therefore, cTn has a tendency to gradually replace enzymatic indicators. The determination of troponin mainly adopts the double antibody sandwich immunological method, and the detection methods include chemiluminescence and electrochemiluminescence.

5%-8% of cTnT is distributed in the cytoplasm of myocardial cells as a free cytoplasmic protein, 92%-95% is bound to thin filaments as a bound structural protein; 3% of cTnI is distributed in the cytoplasm of myocardial cells, and 97% is bound to myocardial structural proteins. When myocardial cells are damaged by ischemia, hypoxia and other factors, free cTnI and cTnT are first rapidly released from the cells into the blood, and then the bound cTnI and cTnT bound to the myocardial structural proteins are gradually decomposed and slowly released into the circulating blood, thus explaining why cTnI and cTnT appear earlier in the circulating blood and can persist for a longer time in diseases manifested by myocardial cell damage, such as acute myocardial infarction (AMI).

What is cardiac troponin? I believe many people have fully understood what cardiac troponin is through the above introduction. After fully understanding it, in order to protect your own health, you can choose to use cardiac troponin under the guidance of a doctor. I believe that by using it, you can also protect your heart and always maintain a healthy state.