Pathogenesis of Chronic Chagas Disease: Macrophages, Mitochondria, and Oxidative Stress

Marcos Lopez, Herbert B. Tanowitz, Nisha J. Garg

    Research output: Contribution to journalReview articlepeer-review

    43 Scopus citations


    Purpose of Review: Trypanosoma cruzi is the causative agent of Chagas disease. Decades after initial infection, ~ 30% of individuals can develop chronic chagasic cardiomyopathy. There are several proposed mechanisms for pathogenesis of Chagas disease, including parasite persistence, immune responses against parasite or self that continue in the heart, vascular compromise, and involvement of autonomic and central nervous system. Herein, we will focus on the significance of macrophages, mitochondrial dysfunction, and oxidative stress in progression of chagasic cardiomyopathy. Recent Findings: The current literature suggests that T. cruzi prevents cytotoxic activities of the innate immune cells and persists in the host, contributing to mitochondrial oxidative stress. We discuss how the neoantigens generated due to cellular oxidative damage contribute to chronic inflammatory stress in chagasic disease. Summary: We propose that metabolic regulators, PARP-1/SIRT1, determine the disease outcome by modulating the mitochondrial and macrophage stress and antioxidant/oxidant imbalance and offer a potential new therapy against chronic Chagas disease.

    Original languageEnglish (US)
    Pages (from-to)45-54
    Number of pages10
    JournalCurrent Clinical Microbiology Reports
    Issue number1
    StatePublished - Mar 1 2018


    • Chagas disease
    • Innate immunity
    • Mitochondrial dysfunction
    • Oxidative stress
    • Reactive oxygen species
    • Trypanosoma cruzi

    ASJC Scopus subject areas

    • Microbiology (medical)
    • Infectious Diseases


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