Evidence map›Paper›PMID 39168268›Full record

ArticleMolecular metabolism2024

Conditional deletion of CEACAM1 in hepatic stellate cells causes their activation.

Harrison T Muturi, Hilda E Ghadieh, Suman Asalla, Sumona G Lester, Getachew D Belew, Sobia Zaidi, Raziyeh Abdolahipour, Abhishek P Shrestha, Agnes O Portuphy, Hannah L Stankus and 10 more

Abstract read
In one paragraph

Article in Molecular metabolism, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Regulation of lipid storage and inflammation in the liver by CEACAM1.European journal of clinical investigation · 2024
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors.

Harrison T MuturiDepartment of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio University, Athens, OH, USA.
Hilda E GhadiehDepartment of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio University, Athens, OH, USA; Department of Biomedical Sciences, University of Balamand, Faculty of Medicine and Health Sciences, Al-Koura, Lebanon.
Suman AsallaDepartment of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio University, Athens, OH, USA.
Sumona G LesterCenter for Diabetes and Endocrine Research, College of Medicine and Life Sciences, University of Toledo, Toledo, OH, USA.
Getachew D BelewDepartment of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio University, Athens, OH, USA.
Sobia ZaidiDepartment of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio University, Athens, OH, USA.
Raziyeh AbdolahipourDepartment of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio University, Athens, OH, USA.
Abhishek P ShresthaDepartment of Surgery, College of Medicine, University of Florida, Gainesville, FL, USA.
Agnes O PortuphyDepartment of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio University, Athens, OH, USA.
Hannah L StankusDepartment of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio University, Athens, OH, USA.
Raghd Abu HelalDepartment of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio University, Athens, OH, USA.
Stefaan VerhulstLiver Cell Biology Research Group, Vrije Universiteit Brussel, Brussel, Belgium.
Sergio DuarteDepartment of Surgery, College of Medicine, University of Florida, Gainesville, FL, USA.
Ali ZarrinparDepartment of Surgery, College of Medicine, University of Florida, Gainesville, FL, USA.
Leo A van GrunsvenLiver Cell Biology Research Group, Vrije Universiteit Brussel, Brussel, Belgium.
Scott L FriedmanDivision of Liver Diseases, Icahn School of Medicine at Mount Sinai, New York 10029, NY, USA.
Robert F SchwabeDepartment of Medicine and the Digestive and Liver Disease Research Center, Columbia University New York, NY, USA.
Terry D HindsDepartment of Pharmacology and Nutritional Sciences, University of Kentucky College of Medicine, Lexington, KY, USA.
Sivarajan KumarasamyDepartment of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio University, Athens, OH, USA.
Sonia M NajjarDepartment of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio University, Athens, OH, USA; Diabetes Institute, Heritage College of Osteopathic Medicine, Ohio University, Athens, OH, USA. Electronic address: najjar@ohio.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesHepatic CEACAM1 expression declines with advanced hepatic fibrosis stage in patients with metabolic dysfunction-associated steatohepatitis (MASH). Global and hepatocyte-specific deletions of Ceacam1 impair insulin clearance to cause hepatic insulin resistance and steatosis. They also cause hepatic inflammation and fibrosis, a condition characterized by excessive collagen production from activated hepatic stellate cells (HSCs). Given the positive effect of PPARγ on CEACAM1 transcription and on HSCs quiescence, the current studies investigated whether CEACAM1 loss from HSCs causes their activation.

methodsWe examined whether lentiviral shRNA-mediated CEACAM1 donwregulation (KD-LX2) activates cultured human LX2 stellate cells. We also generated LratCre + Cc1

resultsLratCre + Cc1

conclusionsLoss of CEACAM1 in HSCs provoked their myofibroblastic transformation in the absence of insulin resistance and hepatic steatosis. This response is mediated by autocrine HSCs activation of the EGFR pathway that amplifies inflammation and proliferation.

Indexed as

Antigens, CDHepatic Stellate CellsAnimalsCarcinoembryonic AntigenCell Adhesion MoleculesGene DeletionHumansLiver CirrhosisMaleMiceMice, Inbred C57BLSignal TransductionAntigens, CDCarcinoembryonic AntigenCD66 antigensCeacam1 protein, mouseCell Adhesion MoleculesHepatic fibrosisHepatic steatosisInflammationRetinoic acidStellate cell proliferation

Identifiers

PMID39168268
PMCPMC11403062

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.