Troponin T and I have been used to study myocardial cell damage due to angina and myocardial infarction. Angina is a condition in which there are sharp chest pains, usually associated with blocked arteries. Troponin T and I have also been used to study the effects transplant rejection, after a heart transplant surgery. Transplant rejection occurs when the new tissues are not accepted by the body’s own tissues and the new tissues are attacked. It is thought that rejection should lead to elevated levels of troponin. This experiment was designed to test whether cell damage due to rejection could be detected based on the levels of troponin. This would be important to determine if there is persistent damage to the cells. The researchers showed that there were indeed elevated levels of troponin to indicate cell damage. This information could be useful in determining how to decrease the risk of rejection of tissues when transplants occur

http://jama.ama-assn.org/content/284/4/457.full.pdf

Structure of the Troponin Complex and Heart Diseases

Cardiovascular disease is the number one cause of death in the United States. Death occurs due to the inability of the heart to distribute blood to the body. This is in turn caused by the inability of the heart of contract. The contraction of the heart is caused by troponin. In this experiment, the researchers were testing the effect that green tea has on the heart and the ability of troponin to bind Ca²⁺. Troponin is a complex made up of two polymers. There is a backbone that is made up of a double helix of actin. On consecutive actin molecules, there is a trimer of troponin C, I and T. Troponin c is the site at which the Ca²⁺ binds. Troponin I is the inhibitory unit of the complex, it serves to regulate the actin-myosin bridge. Troponin T anchors the complex to the filament.  
In this experiment, it was found that drugs that alter the sensitivity of the troponin complex to Ca²⁺ is a safer route than altering the cystolic concentration of Ca²⁺. An increase in sensitivity could increase the amount of Ca that binds to troponin and this causes the heart to contract. Also desensitizers could protect the heart against hypertrophic cardiomyopathy, which is enlargement of the heart. The desensitizers would make the Ca less likely to bind to the troponin and cause an increase in the rate of heart contractions. These sensitizers do not inhibit Ca concentrations, therefore they do not affect homeostasis.

http://www.jbc.org/content/284/34/23012.full

Troponin and the Heart

Troponin is a protein that is present in muscle. It is central to muscle contraction. When calcium channels open, the calcium binds to the troponin, causing a conformational change. This change opens a space that allows actin to bind and begin muscle contraction. Troponin is a component of skeletal and cardiac muscle. Troponin has been used in much research with regard to the heart. In this particular article, the researchers were experimenting with Ca²⁺ sensitizing agents. Cognitive heart failure results when there is desensitization of the heart muscle to Ca²⁺. Ca²⁺ channels are what cause the change in troponin to cause muscle contraction. Ideal sensitizers are compounds that would increase the flux of ions in the channel and create a powerful muscle contraction. Troponin C, one of three types of troponin, is the critical to muscle contraction in the heart. Without this protein, the heart would not be able to contract and blood would fail to be pumped to the body and death would result. This protein is crucial for the beating of the heart. (lub dub)

http://www.jbc.org/content/274/34/23932.full.pdf