Evidence map›Paper›PMID 33826636›Full record

ArticlePLoS neglected tropical diseases2021

Fat tissue regulates the pathogenesis and severity of cardiomyopathy in murine chagas disease.

Kezia Lizardo, Janeesh P Ayyappan, Neelam Oswal, Louis M Weiss, Philipp E Scherer, Jyothi F Nagajyothi

Abstract read
In one paragraph

Article in PLoS neglected tropical diseases, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

  1. Article
  2. Coinfection by multipleMicrobiology and molecular biology reviews : MMBR · 2025
    Review
  3. Review
  4. Review
  5. Article
  6. The intersection of hostMicrobiology and molecular biology reviews : MMBR · 2024
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Sex Differences in Cardiac Pathology of SARS-CoV2 Infected andFrontiers in cardiovascular medicine · 2022
    Article
  16. Review
  17. 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

6 authors.

Kezia LizardoCenter for Discovery and Innovation, Hackensack University Medical Center, Nutley, New Jersey, United States of America.
Janeesh P AyyappanDepartment of Biochemisty, University of Kerala, Kerala, India.
Neelam OswalCenter for Discovery and Innovation, Hackensack University Medical Center, Nutley, New Jersey, United States of America.
Louis M WeissDepartment of Pathology, Albert Einstein College of Medicine, Bronx, New York, New York, United States of America.ORCID 0000-0002-0357-7396
Philipp E SchererThe Touchstone Diabetes Center, UT Southwestern Medical Center, Dallas, Texas, United States of America.ORCID 0000-0003-0680-3392
Jyothi F NagajyothiCenter for Discovery and Innovation, Hackensack University Medical Center, Nutley, New Jersey, United States of America.ORCID 0000-0003-3541-779X

Funding

Pathogenic contribution of lipid homeostasis to chagasic CardiomyopathyR01HL122866 · NHLBI · RBHS-NEW JERSEY MEDICAL SCHOOL · PI NAGAJYOTHI, JYOTHI FALGUNI · 2015 to 2018
$1.6M
NHLBI NIH HHS R01 HL122866
6 · The paper itself

Abstract

Chronic Chagas cardiomyopathy (CCC) caused by a parasite Trypanosoma cruzi is a life-threatening disease in Latin America, for which there is no effective drug or vaccine. The pathogenesis of CCC is complex and multifactorial. Previously, we demonstrated T. cruzi infected mice lose a significant amount of fat tissue which correlates with progression of CCC. Based on this an investigation was undertaken during both acute and chronic T. cruzi infection utilizing the FAT-ATTAC murine model (that allows modulation of fat mass) to understand the consequences of the loss of adipocytes in the regulation of cardiac parasite load, parasite persistence, inflammation, mitochondrial stress, ER stress, survival, CCC progression and CCC severity. Mice were infected intraperitoneally with 5x104 and 103 trypomastigotes to generate acute and chronic Chagas models, respectively. Ablation of adipocytes was carried out in uninfected and infected mice by treatment with AP21087 for 10 days starting at 15DPI (acute infection) and at 65DPI (indeterminate infection). During acute infection, cardiac ultrasound imaging, histological, and biochemical analyses demonstrated that fat ablation increased cardiac parasite load, cardiac pathology and right ventricular dilation and decreased survival. During chronic indeterminate infection ablation of fat cells increased cardiac pathology and caused bi-ventricular dilation. These data demonstrate that dysfunctional adipose tissue not only affects cardiac metabolism but also the inflammatory status, morphology and physiology of the myocardium and increases the risk of progression and severity of CCC in murine Chagas disease.

Indexed as

AdipogenesisAdipose Tissue, WhiteAnimalsChagas CardiomyopathyCholesterol, LDLDiet, High-FatDisease Models, AnimalFemaleLipid MetabolismMaleMiceMice, Inbred C3HMyocarditisMyocardiumParasite LoadUltrasonography, DopplerCholesterol, LDL

Identifiers

PMID33826636
PMCPMC8055007

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.