ArticleNature communications2018
Canonical PI3Kγ signaling in myeloid cells restricts Trypanosoma cruzi infection and dampens chagasic myocarditis.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Targeting macrophage phenotypes to prevent diseases caused byFrontiers in immunology · 2025Review
- Cardiac and Digestive Forms of Chagas Disease: An Update on Pathogenesis, Genetics, and Therapeutic Targets.Mediators of inflammation · 2025Review
- Therapeutic potential of anti-PIK3CG treatment for multiple myeloma via inhibiting c-Myc pathway.Heliyon · 2024Article
- Differential cardiomyocyte transcriptomic remodeling during in vitro Trypanosoma cruzi infection using laboratory strains provides implications on pathogenic host responses.Tropical medicine and health · 2023Article
- Anti-Trypanosoma cruzi activity of Coptis rhizome extract and its constituents.Tropical medicine and health · 2023Article
- Immunopathogenesis inFrontiers in immunology · 2023Review
- PI3K signalling at the intersection of cardio-oncology networks: cardiac safety in the era of AI.Cellular and molecular life sciences : CMLS · 2022Review
- The role of PI3Kγ in the immune system: new insights and translational implications.Nature reviews. Immunology · 2022Review
- Impact of IFN-γ Deficiency on the Cardiomyocyte Function in the First Stage of Experimental Chagas Disease.Microorganisms · 2022Article
- Observational
- Transcriptional Studies onFrontiers in cellular and infection microbiology · 2021Review
- Gene expression network analyses during infection with virulent and avirulent Trypanosoma cruzi strains unveil a role for fibroblasts in neutrophil recruitment and activation.PLoS pathogens · 2020Article
- Quantification of parasite burden of Trypanosoma cruzi and identification of Discrete Typing Units (DTUs) in blood samples of Latin American immigrants residing in Barcelona, Spain.PLoS neglected tropical diseases · 2020Article
- Pyridinecarboxylic Acid Derivative Stimulates Pro-Angiogenic Mediators by PI3K/AKT/mTOR and Inhibits Reactive Nitrogen and Oxygen Species and NF-κB Activation Through a PPARγ-Dependent Pathway inFrontiers in immunology · 2019Article
- Search of Allosteric Inhibitors and Associated Proteins of an AKT-International journal of molecular sciences · 2018Article
- Disease Tolerance and Pathogen Resistance Genes May UnderlieFrontiers in immunology · 2018Article
Corrections and comments
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Authors and funding
22 authors at 6 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chagas disease is caused by infection with the protozoan Trypanosoma cruzi (T. cruzi) and is an important cause of severe inflammatory heart disease. However, the mechanisms driving Chagas disease cardiomyopathy have not been completely elucidated. Here, we show that the canonical PI3Kγ pathway is upregulated in both human chagasic hearts and hearts of acutely infected mice. PI3Kγ-deficient mice and mutant mice carrying catalytically inactive PI3Kγ are more susceptible to T. cruzi infection. The canonical PI3Kγ signaling in myeloid cells is essential to restrict T. cruzi heart parasitism and ultimately to avoid myocarditis, heart damage, and death of mice. Furthermore, high PIK3CG expression correlates with low parasitism in human Chagas' hearts. In conclusion, these results indicate an essential role of the canonical PI3Kγ signaling pathway in the control of T. cruzi infection, providing further insight into the molecular mechanisms involved in the pathophysiology of chagasic heart disease.
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