Evidence map›Paper›PMID 27054331›Full record

ArticleCell death & disease2016

PER1 prevents excessive innate immune response during endotoxin-induced liver injury through regulation of macrophage recruitment in mice.

T Wang, Z Wang, P Yang, L Xia, M Zhou, S Wang, Jie Du, J Zhang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 16% of its field
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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.

  1. Pooled it
  2. Circadian rhythms and lung cancer biology and immunotherapy: Emerging opportunities and challenges.Chinese medical journal pulmonary and critical care medicine · 2026
    Review
  3. Review
  4. Inhibition of Circadian Rhythm GeneEnvironment & health (Washington, D.C.) · 2025
    Article
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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

8 authors at 4 institutions in 1 country.

T WangCenter for Molecular Metabolism, Nanjing University of Science and Technology, Nanjing, China.
Z WangDepartment of Radiology, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China.
P YangCenter for Molecular Metabolism, Nanjing University of Science and Technology, Nanjing, China.
L XiaCenter for Molecular Metabolism, Nanjing University of Science and Technology, Nanjing, China.
M ZhouCenter for Molecular Metabolism, Nanjing University of Science and Technology, Nanjing, China.
S WangCenter for Molecular Metabolism, Nanjing University of Science and Technology, Nanjing, China.
Jie DuBeijing An Zhen Hospital, Capital Medical University, Beijing, China.
J ZhangCenter for Molecular Metabolism, Nanjing University of Science and Technology, Nanjing, China.
Nanjing University of Science and Technology · CNBeijing Anzhen Hospital · CNNanjing University of Chinese Medicine · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The severity of acute liver failure (ALF) induced by bacterial lipopolysaccharide (LPS) is associated with the hepatic innate immune response. The core circadian molecular clock modulates the innate immune response by controlling rhythmic pathogen recognition by the innate immune system and daily variations in cytokine gene expression. However, the molecular link between circadian genes and the innate immune system has remained unclear. Here, we showed that mice lacking the clock gene Per1 (Period1) are more susceptible to LPS/d-galactosamine (LPS/GalN)-induced macrophage-dependent ALF compared with wild-type (WT) mice. Per1 deletion caused a remarkable increase in the number of Kupffer cells (KCs) in the liver, resulting in an elevation of the levels of pro-inflammatory cytokines after LPS treatment. Loss of Per1 had no effect on the proliferation or apoptosis of macrophages; however, it enhanced the recruitment of macrophages, which was associated with an increase in CC chemokine receptor 2 (Ccr2) expression levels in monocytes/macrophages. Deletion of Ccr2 rescued d-GalN/LPS-induced liver injury in Per1(-/-) mice. We demonstrated that the upregulation of Ccr2 expression by Per1 deletion could be reversed by the synthetic peroxisome proliferator-activated receptor gamma (PPAR-γ) antagonist GW9662. Further analysis indicated that PER1 binds to PPAR-γ on the Ccr2 promoter and enhanced the inhibitory effect of PPAR-γ on Ccr2 expression. These results reveal that Per1 reduces hepatic macrophage recruitment through interaction with PPAR-γ and prevents an excessive innate immune response in endotoxin-induced liver injury.

Indexed as

Immunity, InnateAnilidesAnimalsCell MovementChemokinesCytokinesGalactosamineKupffer CellsLipopolysaccharidesLiverLiver Failure, AcuteMacrophagesMaleMiceMice, Inbred C57BLMice, Knockout2-chloro-5-nitrobenzanilideAnilidesChemokinesCytokinesGalactosamineLipopolysaccharidesPer1 protein, mousePeriod Circadian ProteinsPPAR gammaReceptors, CCR2

Identifiers

PMID27054331
PMCPMC4855679
OpenAlexW2318781120

What OpenQuestion 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 OpenQuestion graph.