In the absence of mechanisms controlling initiation of transcription, extracellular signals will trigger subsets of Trypanosoma cruzi genes to be post-transcriptionally co-regulated.
[6] During smooth muscle cell invasion, cruzipain may mobilize vasoconstricting endothelin receptors, which may interfere with the vasoconstrictor's ability to cause the blood vessels to become narrower.
Results have been found using a cruzipain DNA-based vaccine that has demonstrated a decrease in parasitemia, inflammatory cell infiltrate, and tissue damage in models of infection caused by Trypanosoma cruzi.
In the experiment, chagasin, a natural protein of Trypanosoma cruzi, and a tight binding inhibitor of papain-like cysteine proteases is used.
Both of these drugs require long use, cause adverse side effects, and have controversial efficacy in adults infected with Trypanosoma cruzi.
These drugs showed the ability to inhibit cruzipain, by diminishing the burden of the parasite in skeletal and cardiac muscles, as well as by reducing the inflammatory response in the tissues of Trypanosoma cruzi infected mice.