ArticlePloS one2011
Heme-induced ROS in Trypanosoma cruzi activates CaMKII-like that triggers epimastigote proliferation. One helpful effect of ROS.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 54 citations in OpenAlex.
- The heme A synthase Cox15, as a target of redox-active 3-benzylmenadiones with antiparasitic activity.Antimicrobial agents and chemotherapy · 2026Article
- Translesion synthesis and microhomology-mediated end-joining repair in trypanosomatids.PLoS neglected tropical diseases · 2025Review
- Heart function enhancement by an Nrf2-activating antioxidant in acute Y-strain Chagas disease, but not in chronic Colombian or Y-strain.PLoS neglected tropical diseases · 2024Article
- Review
- α-Glucosidase isoform G contributes to heme detoxification inCurrent research in insect science · 2024Article
- CaMKII regulates neuromuscular activity and survival of the human blood fluke Schistosoma mansoni.Scientific reports · 2022Article
- The Kinetoplastid-Specific Protein TcCAL1 Plays Different Roles DuringFrontiers in cellular and infection microbiology · 2022Article
- Intrinsic and Chemotherapeutic Stressors Modulate ABCC-Like Transport inMolecules (Basel, Switzerland) · 2021Article
- An Overview on the Therapeutics of Neglected Infectious Diseases-Leishmaniasis and Chagas Diseases.Frontiers in chemistry · 2021Review
- Dual and Opposite Roles of Reactive Oxygen Species (ROS) in Chagas Disease: Beneficial on the Pathogen and Harmful on the Host.Oxidative medicine and cellular longevity · 2020Review
- Gene expression profiling of Trypanosoma cruzi in the presence of heme points to glycosomal metabolic adaptation of epimastigotes inside the vector.PLoS neglected tropical diseases · 2020Article
- Metabolic syndrome agravates cardiovascular, oxidative and inflammatory dysfunction during the acute phase of Trypanosoma cruzi infection in mice.Scientific reports · 2019Article
- Bioactive lipids regulate Trypanosoma cruzi development.Parasitology research · 2019Article
- Redox Balance Keepers and Possible Cell Functions Managed by Redox Homeostasis inFrontiers in cellular and infection microbiology · 2019Review
- Heme crystallization in a Chagas disease vector acts as a redox-protective mechanism to allow insect reproduction and parasite infection.PLoS neglected tropical diseases · 2018Article
- Review
- Physiological and unappreciated roles of CaMKII in the heart.Basic research in cardiology · 2018Review
- ROS and Trypanosoma cruzi: Fuel to infection, poison to the heart.PLoS pathogens · 2018Review
- The superfamily keeps growing: Identification in trypanosomatids of RibJ, the first riboflavin transporter family in protists.PLoS neglected tropical diseases · 2017Article
- Catalase protects Aedes aegypti from oxidative stress and increases midgut infection prevalence of Dengue but not Zika.PLoS neglected tropical diseases · 2017Article
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heme is a ubiquitous molecule that has a number of physiological roles. The toxic effects of this molecule have been demonstrated in various models, based on both its pro-oxidant nature and through a detergent mechanism. It is estimated that about 10 mM of heme is released during blood digestion in the blood-sucking bug's midgut. The parasite Trypanosoma cruzi, the agent of Chagas' disease, proliferates in the midgut of the insect vector; however, heme metabolism in trypanosomatids remains to be elucidated. Here we provide a mechanistic explanation for the proliferative effects of heme on trypanosomatids. Heme, but not other porphyrins, induced T. cruzi proliferation, and this phenomenon was accompanied by a marked increase in reactive oxygen species (ROS) formation in epimastigotes when monitored by ROS-sensitive fluorescent probes. Heme-induced ROS production was time- and concentration-dependent. In addition, lipid peroxidation and the formation of 4-hydroxy-2-nonenal (4-HNE) adducts with parasite proteins were increased in epimastigotes in the presence of heme. Conversely, the antioxidants urate and GSH reversed the heme-induced ROS. Urate also decreased parasite proliferation. Among several protein kinase inhibitors tested only specific inhibitors of CaMKII, KN93 and Myr-AIP, were able to abolish heme-induced ROS formation in epimastigotes leading to parasite growth impairment. Taken together, these data provide new insight into T. cruzi- insect vector interactions: heme, a molecule from the blood digestion, triggers epimastigote proliferation through a redox-sensitive signalling mechanism.
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