Evidence map›Paper›PMID 38062533›Full record

ArticleTropical medicine and health2023

Differential cardiomyocyte transcriptomic remodeling during in vitro Trypanosoma cruzi infection using laboratory strains provides implications on pathogenic host responses.

Katherine-Sofia Candray-Medina, Yu Nakagama, Masamichi Ito, Shun Nakagama, Evariste Tshibangu-Kabamba, Norihiko Takeda, Yuki Sugiura, Yuko Nitahara, Yu Michimuko-Nagahara, Natsuko Kaku and 9 more

Abstract read
In one paragraph

Article in Tropical medicine and health, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. Coinfection by multipleMicrobiology and molecular biology reviews : MMBR · 2025
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

19 authors.

Katherine-Sofia Candray-MedinaDepartment of Parasitology, Graduate School of Medicine, Osaka Metropolitan University, 1-4-3 Asahi-machi, Abeno-ku, Osaka, 545-8585, Japan.
Yu NakagamaDepartment of Parasitology, Graduate School of Medicine, Osaka Metropolitan University, 1-4-3 Asahi-machi, Abeno-ku, Osaka, 545-8585, Japan. ynakagama@gmail.com.ORCID http://orcid.org/0000-0001-9780-9719
Masamichi ItoDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan.
Shun NakagamaDepartment of Cardiovascular Medicine, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8519, Japan.
Evariste Tshibangu-KabambaDepartment of Parasitology, Graduate School of Medicine, Osaka Metropolitan University, 1-4-3 Asahi-machi, Abeno-ku, Osaka, 545-8585, Japan.
Norihiko TakedaDivision of Cardiology and Metabolism, Center for Molecular Medicine, Jichi Medical University, 3311-1 Yakushiji, Shimotsuke, 329-0498, Japan.
Yuki SugiuraCenter for Cancer Immunotherapy and Immunobiology, Kyoto University Graduate School of Medicine, Yoshida Nihonmatsucho, Sakyo-ku, Kyoto, 606-8501, Japan.
Yuko NitaharaDepartment of Parasitology, Graduate School of Medicine, Osaka Metropolitan University, 1-4-3 Asahi-machi, Abeno-ku, Osaka, 545-8585, Japan.
Yu Michimuko-NagaharaDepartment of Parasitology, Graduate School of Medicine, Osaka Metropolitan University, 1-4-3 Asahi-machi, Abeno-ku, Osaka, 545-8585, Japan.
Natsuko KakuDepartment of Parasitology, Graduate School of Medicine, Osaka Metropolitan University, 1-4-3 Asahi-machi, Abeno-ku, Osaka, 545-8585, Japan.
Yoko OnizukaDepartment of Molecular and Cellular Parasitology, Graduate School of Health Sciences, Gunma University, 3-39-22 Showa-machi, Maebashi, Gunma, 371-8514, Japan.
Carmen-Elena AriasCentro Nacional de Investigaciones Científicas de El Salvador (CICES), Ciudad Universitaria "Dr. Fabio Castillo Figueroa", final avenida "Mártires del 30 de julio", San Salvador, El Salvador.
Maricela MejiaCentro Nacional de Investigaciones Científicas de El Salvador (CICES), Ciudad Universitaria "Dr. Fabio Castillo Figueroa", final avenida "Mártires del 30 de julio", San Salvador, El Salvador.
Karla AlasCentro Nacional de Investigaciones Científicas de El Salvador (CICES), Ciudad Universitaria "Dr. Fabio Castillo Figueroa", final avenida "Mártires del 30 de julio", San Salvador, El Salvador.
Susana PeñaDepartamento de Investigación, Hospital Nacional Especializado "Rosales", Ministerio de Salud de El Salvador, Calle Arce No. 827, San Salvador, El Salvador.
Yasuhiro MaejimaDepartment of Cardiovascular Medicine, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8519, Japan.
Issei KomuroInternational University of Health and Welfare, Minato-Ku, Tokyo, 107-8402, Japan.
Junko Nakajima-ShimadaDepartment of Molecular and Cellular Parasitology, Graduate School of Health Sciences, Gunma University, 3-39-22 Showa-machi, Maebashi, Gunma, 371-8514, Japan.
Yasutoshi KidoDepartment of Parasitology, Graduate School of Medicine, Osaka Metropolitan University, 1-4-3 Asahi-machi, Abeno-ku, Osaka, 545-8585, Japan.

Funding

Japan Agency for Medical Research and Development JP21jm0110016Japan Agency for Medical Research and Development JP21wm0325049Japan Society for the Promotion of Science 19K23992Platform for advanced genome science 16H06279
6 · The paper itself

Abstract

backgroundChagas disease can lead to life-threatening cardiac manifestations. Regional factors, including genetic characteristics of circulating Trypanosoma cruzi (T. cruzi), have attracted attention as likely determinants of Chagas disease phenotypic expression and Chagas cardiomyopathy (CCM) progression. Our objective was to elucidate the differential transcriptomic signatures of cardiomyocytes resulting from infection with genetically discrete T. cruzi strains and explore their relationships with CCM pathogenesis and progression.

methodsHL-1 rodent cardiomyocytes were infected with T. cruzi trypomastigotes of the Colombian, Y, or Tulahuen strain. RNA was serially isolated post-infection for microarray analysis. Enrichment analyses of differentially expressed genes (fold-change ≥ 2 or ≤ 0.5) highlighted over-represented biological pathways. Intracellular levels of reactive oxygen species (ROS) were compared between T. cruzi-infected and non-infected HL-1 cardiomyocytes.

resultsWe found that oxidative stress-related gene ontology terms (GO terms), 'Hypertrophy model', 'Apoptosis', and 'MAPK signaling' pathways (all with P < 0.01) were upregulated. 'Glutathione and one-carbon metabolism' pathway, and 'Cellular nitrogen compound metabolic process' GO term (all with P < 0.001) were upregulated exclusively in the cardiomyocytes infected with the Colombian/Y strains. Mean intracellular levels of ROS were significantly higher in the T. cruzi-infected cardiomyocytes compared to the non-infected (P < 0.0001).

conclusionsThe upregulation of oxidative stress-related and hypertrophic pathways constitutes the universal hallmarks of the cardiomyocyte response elicited by T. cruzi infection. Nitrogen metabolism upregulation and glutathione metabolism imbalance may implicate a relationship between nitrosative stress and poor oxygen radicals scavenging in the unique pathophysiology of Chagas cardiomyopathy.

Indexed as

Chagas diseaseDilated cardiomyopathyGlutathione metabolismHL-1In vitro modelingNeglected tropical diseasesOxidative stressTranscriptomeTrypanosoma cruzi

Identifiers

PMID38062533
PMCPMC10702087

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.