Evidence map›Paper›PMID 39104322›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2024

A novel mouse model of hepatocyte-specific apoptosis-induced myeloid cell-dominant sterile liver injury and repair response.

Heng-Fu Bu, Saravanan Subramanian, Pauline M Chou, Fangyi Liu, Leyu Sun, Hua Geng, Xiao Wang, Jie Liao, Chao Du, Joyce Hu and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

14 authors.

Heng-Fu BuDepartment of Pediatrics, Pediatric Mucosal Inflammation and Regeneration Research Program, Center for Pediatric Translational Research and Education, College of Medicine, University of Illinois at Chicago, Chicago, Illinois, United States.
Saravanan SubramanianDepartment of Pediatrics, Pediatric Mucosal Inflammation and Regeneration Research Program, Center for Pediatric Translational Research and Education, College of Medicine, University of Illinois at Chicago, Chicago, Illinois, United States.
Pauline M ChouDepartment of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, United States.ORCID 0000-0002-1114-8305
Fangyi LiuDepartment of Pediatrics, Pediatric Mucosal Inflammation and Regeneration Research Program, Center for Pediatric Translational Research and Education, College of Medicine, University of Illinois at Chicago, Chicago, Illinois, United States.
Leyu SunDepartment of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, United States.
Hua GengDepartment of Pediatrics, Pediatric Mucosal Inflammation and Regeneration Research Program, Center for Pediatric Translational Research and Education, College of Medicine, University of Illinois at Chicago, Chicago, Illinois, United States.
Xiao WangDepartment of Pediatrics, Pediatric Mucosal Inflammation and Regeneration Research Program, Center for Pediatric Translational Research and Education, College of Medicine, University of Illinois at Chicago, Chicago, Illinois, United States.
Jie LiaoDepartment of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, United States.
Chao DuDepartment of Pediatrics, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, United States.
Joyce HuDepartment of Pediatrics, Pediatric Mucosal Inflammation and Regeneration Research Program, Center for Pediatric Translational Research and Education, College of Medicine, University of Illinois at Chicago, Chicago, Illinois, United States.
Stephanie C TanDepartment of Pediatrics, Pediatric Mucosal Inflammation and Regeneration Research Program, Center for Pediatric Translational Research and Education, College of Medicine, University of Illinois at Chicago, Chicago, Illinois, United States.
Nirmal NathanDepartment of Pediatrics, Pediatric Mucosal Inflammation and Regeneration Research Program, Center for Pediatric Translational Research and Education, College of Medicine, University of Illinois at Chicago, Chicago, Illinois, United States.
Guang-Yu YangDepartment of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, United States.
Xiao-Di TanDepartment of Pediatrics, Pediatric Mucosal Inflammation and Regeneration Research Program, Center for Pediatric Translational Research and Education, College of Medicine, University of Illinois at Chicago, Chicago, Illinois, United States.ORCID 0000-0003-3766-5885

Funding

Insights into a multi-hit process in the development of necrotizing enterocolitisR01DK129960 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI TAN, XIAO-DI · 2022 to 2025
$2.6M
Mechanisms underlying regulation of intestinal epithelial homeostasis in sepsisR01DK123826 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI TAN, XIAO-DI · 2020 to 2023
$2.4M
Role of epoxy fatty acids - soluble epoxide hydrolase axis in intestinal mucosal barrier defenseR01DK137885 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI Guang-Yu Yang · 2024 to 2026
$1.8M
Milk fat globule-EGF factor 8 and hepatocyte apoptosis-induced liver wound healing responseI01BX006085 · VA · JESSE BROWN VA MEDICAL CENTER · PI Xiao-Di Tan · 2023 to 2026
–
BLRD VA I01 BX006085HHS | NIH | NIDDK | Division of Diabetes, Endocrinology, and Metabolic Diseases (DEM) 137885HHS | NIH | NIDDK | Division of Diabetes, Endocrinology, and Metabolic Diseases (DEM) DK123826HHS | NIH | NIDDK | Division of Diabetes, Endocrinology, and Metabolic Diseases (DEM) DK129960NIDDK NIH HHS R01 DK123826NIDDK NIH HHS R01 DK129960U.S. Department of Veterans Affairs (VA) I01BX006085
6 · The paper itself

Abstract

Apoptosis, inflammation, and wound healing are critical pathophysiological events associated with various liver diseases. Currently, there is a lack of in vivo approaches to study hepatocyte apoptosis-induced liver injury and repair. To address this critical knowledge gap, we developed a unique genetically modified mouse model, namely, 3-Transgene (Tg) with inducible Hepatocyte-Specific Apoptosis Phenotype (3xTg-iHAP) in this study. The 3xTg-iHAP mice possess three transgenes including

Indexed as

ApoptosisDisease Models, AnimalHepatocytesLiver RegenerationMice, TransgenicMyeloid CellsAnimalsChemokine CXCL1LiverMiceMice, Inbred C57BLWound HealingChemokine CXCL1Cxcl1 protein, mouseliver wound healingmouse model for liver wound healingregenerationsterile liver inflammation

Identifiers

PMID39104322
PMCPMC11482258

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.