Mitochondrial involvement in chronic chagasic cardiomyopathy.

Area of Science:

• Cardiovascular Biology
• Parasitology
• Mitochondrial Medicine

Background:

• The exact mechanisms driving chronic Chagasic cardiopathy remain unclear.
• Inflammation and its mediators are suspected to directly harm cardiac cells.

Purpose of the Study:

• To investigate cardiac mitochondrial structure and function in chronic Chagasic myocardiopathy.
• To compare the effects of different Trypanosoma cruzi strains on cardiac mitochondria.

Main Methods:

• Studied mitochondrial structure and enzyme activity (citrate synthase, respiratory chain complexes I-IV) in mice infected with T. cruzi (Tulahuen or SGO Z12 strains) 365 days post-infection.
• Assessed parasite presence in cardiac and skeletal muscle.

Main Results:

• Complexes I-IV activity was altered differently by each T. cruzi strain (P<0.0001).
• Mitochondrial cristae disorganization and parasite persistence were noted in the Tulahuen group.
• Citrate synthase activity increased in both infected groups; mitochondrial structural changes occurred in 89% (Tulahuen) and 58% (SGO Z12) of mice.

Conclusions:

• Parasite persistence and inflammation contribute to cardiac mitochondrial structural and functional alterations in chronic Chagas disease.
• The specific T. cruzi strain dictates the nature of mitochondrial changes observed in chagasic cardiopathy.