Atlas offers closer look at CHF damage
Atlas offers closer look at CHF damage
The major structural characteristic of CHF is myocardial cell death that occurs through cell necrosis and apoptosis.
Regardless of initial cause, the disease, once initiated, worsens even in the absence of additional injury, suggesting a self-amplifying reaction initially triggered by pump failure.
Three proteins comprise the troponin complex:
1. troponin C, calcium-binding protein;
2. TnT, tropomyosin-binding protein;
3. troponin I, inhibitory protein.
All three proteins regulate the calcium-dependent interaction between actin and myosin in striated muscle. TnT is tightly anchored to the troponin-tropomyosin complex around the actin filament in the contractile machinery of the heart and, as such, is a well-documented biochemical marker of myocardial injury.
Because it is found only in the heart, increased concentrations of cardiac TnT clearly indicate myocardial cell necrosis — ongoing injury to the heart — and may provide important clinical diagnostic or therapeutic information.
Cardiac contraction is brought about by interactions between actin in the thin filament and myosin cross-bridges that project from the thick filament. (See illustration, below.)
¤ In relaxed muscle, where troponin C (TnC) is not bound to calcium, the "relaxed" conformation of the troponin complexes and tropomyosin prevents actin in the thin filament from interacting with the myosin cross-bridges. As a result, actin is unable to convert the chemical energy of the adenosine triphosphate (ATP) bound to the myosin cross-bridges into mechanical work.
¤ In active muscle, Ca2+ bound to TnC has shifted the troponin complexes and tropomyosin to an "active" conformation that enables actin to interact with the myosin cross-bridges. Release of chemical energy when actin stimulates hydrolysis of myosin-bound ATP enables the cross-bridges to "row" the thin filaments toward the center of the sarcomere.
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