ArticleJournal of the American Heart Association2013
MnSODtg mice control myocardial inflammatory and oxidative stress and remodeling responses elicited in chronic Chagas disease.
Article in Journal of the American Heart Association, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 29 citations in OpenAlex.
- Platelets, Macrophages, and Thromboinflammation in Chagas Disease.Journal of inflammation research · 2022Review
- Use of a small molecule integrin activator as a systemically administered vaccine adjuvant in controlling Chagas disease.NPJ vaccines · 2021Article
- Sirtuin Control of Mitochondrial Dysfunction, Oxidative Stress, and Inflammation in Chagas Disease Models.Frontiers in cellular and infection microbiology · 2021Review
- Epidemiology and pathogenesis of maternal-fetal transmission of Trypanosoma cruzi and a case for vaccine development against congenital Chagas disease.Biochimica et biophysica acta. Molecular basis of disease · 2020Review
- Article
- Immunity and vaccine development efforts against Trypanosoma cruzi.Acta tropica · 2019Review
- Manganese superoxide dismutase deficiency exacerbates the mitochondrial ROS production and oxidative damage in Chagas disease.PLoS neglected tropical diseases · 2018Article
- ROS and Trypanosoma cruzi: Fuel to infection, poison to the heart.PLoS pathogens · 2018Review
- Inhibition of NFE2L2-Antioxidant Response Element Pathway by Mitochondrial Reactive Oxygen Species Contributes to Development of Cardiomyopathy and Left Ventricular Dysfunction in Chagas Disease.Antioxidants & redox signaling · 2017Article
- Gene Expression Profiling and Functional Characterization of Macrophages in Response to Circulatory Microparticles Produced during Trypanosoma cruzi Infection and Chagas Disease.Journal of innate immunity · 2017Article
- SIRT1-PGC1α-NFκB Pathway of Oxidative and Inflammatory Stress during Trypanosoma cruzi Infection: Benefits of SIRT1-Targeted Therapy in Improving Heart Function in Chagas Disease.PLoS pathogens · 2016Article
- Chemotherapeutic efficacy of phosphodiesterase inhibitors in chagasic cardiomyopathy.JACC. Basic to translational science · 2016Article
- Developments in the management of Chagas cardiomyopathy.Expert review of cardiovascular therapy · 2015Review
- Article
- Hepatotoxicity in mice of a novel anti-parasite drug candidate hydroxymethylnitrofurazone: a comparison with Benznidazole.PLoS neglected tropical diseases · 2014Article
- High fat diet modulates Trypanosoma cruzi infection associated myocarditis.PLoS neglected tropical diseases · 2014Article
- Pathogenesis of chagas cardiomyopathy: role of inflammation and oxidative stress.Journal of the American Heart Association · 2013Article
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5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundWe utilized genetically modified mice equipped with a variable capacity to scavenge mitochondrial and cellular reactive oxygen species to investigate the pathological significance of oxidative stress in Chagas disease. METHODS AND
resultsC57BL/6 mice (wild type, MnSODtg, MnSOD+/-, GPx1-/-) were infected with Trypanosoma cruzi and harvested during the chronic disease phase. Chronically infected mice exhibited a substantial increase in plasma levels of inflammatory markers (nitric oxide, myeloperoxidase), lactate dehydrogenase, and myocardial levels of inflammatory infiltrate and oxidative adducts (malondialdehyde, carbonyls, 3-nitrotyrosine) in the order of wild type = MnSOD+/- > GPx1-/- > MnSODtg. Myocardial mitochondrial damage was pronounced and associated with a > 50% decline in mitochondrial DNA content in chronically infected wild-type and GPx1(-/-) mice. Imaging of intact heart for cardiomyocytes and collagen by the nonlinear optical microscopy techniques of multiphoton fluorescence/second harmonic generation showed a significant increase in collagen (> 10-fold) in chronically infected wild-type mice, whereas GPx1-/- mice exhibited a basal increase in collagen that did not change during the chronic phase. Chronically infected MnSODtg mice exhibited a marginal decline in mitochondrial DNA content and no changes in collagen signal in the myocardium. P47phox-/- mice lacking phagocyte-generated reactive oxygen species sustained a low level of myocardial oxidative stress and mitochondrial DNA damage in response to Trypanosoma cruzi infection. Yet chronically infected p47phox-/- mice exhibited increase in myocardial inflammatory and remodeling responses, similar to that noted in chronically infected wild-type mice.
conclusionsInhibition of oxidative burst of phagocytes was not sufficient to prevent pathological cardiac remodeling in Chagas disease. Instead, enhancing the mitochondrial reactive oxygen species scavenging capacity was beneficial in controlling the inflammatory and oxidative pathology and the cardiac remodeling responses that are hallmarks of chronic Chagas disease.
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