Evidence map›Paper›PMID 38799573›Full record

ArticleiScience2024

IGF2BP3 modified GLI2 transcriptionally regulates SYVN1 and facilitates sepsis liver injury through autophagy.

Chuanzheng Sun, Min Gao, Haotian Hu, Jing Qi, Yishu Tang, Xiaoxue Cao, Runbang Zhang, Huaizheng Liu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Research advances in mFrontiers in cell and developmental biology · 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

8 authors.

Chuanzheng SunDepartment of Emergency, The Third Xiangya Hospital, Central South University, Changsha 410013, Hunan Province, P.R. China.
Min GaoDepartment of Critical Care Medicine, The Third Xiangya Hospital, Central South University, Changsha 410013, Hunan Province, P.R. China.
Haotian HuDepartment of Emergency, The Third Xiangya Hospital, Central South University, Changsha 410013, Hunan Province, P.R. China.
Jing QiDepartment of Emergency, The Third Xiangya Hospital, Central South University, Changsha 410013, Hunan Province, P.R. China.
Yishu TangDepartment of Emergency, The Third Xiangya Hospital, Central South University, Changsha 410013, Hunan Province, P.R. China.
Xiaoxue CaoDepartment of Emergency, The Third Xiangya Hospital, Central South University, Changsha 410013, Hunan Province, P.R. China.
Runbang ZhangDepartment of Emergency, The Third Xiangya Hospital, Central South University, Changsha 410013, Hunan Province, P.R. China.
Huaizheng LiuDepartment of Emergency, The Third Xiangya Hospital, Central South University, Changsha 410013, Hunan Province, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy enhancement in septic liver injury can play a protective role. Nerveless, the mechanism of autophagy-mediated septic liver injury needs further investigation. Our study demonstrated that in septic condition, GLI Family Zinc Finger 2 (GLI2) was elevated, whereas peroxisome-proliferator-activated receptor α (PPARα) was downregulated. Suppressing GLI2 or synovialapoptosis inhibitor 1 (SYVN1) in LPS-exposed cells increased PPARα levels, enhanced cell viability and autophagy, while inhibiting apoptosis. LPS enhanced the GLI2-SYVN1 promoter binding. SYVN1 fostered ubiquitin-mediated degradation of PPARα. IGF2BP3 stabilized GLI2 mRNA by targeting its m

Indexed as

cell biologyhepatologyimmunology

Identifiers

PMID38799573
PMCPMC11126807

What OpenQuestion holds

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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.