Evidence map›Paper›PMID 33312380›Full record

ArticleAmerican journal of translational research2020

Downregulation of SENP1 suppresses LPS-induced macrophage inflammation by elevating Sp3 SUMOylation and disturbing Sp3-NF-κB interaction.

Chongwei Zheng, Dongxin Li, Weifeng Zhan, Kairan He, Hang Yang

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2020. 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
0.6field-weighted citation impact, top 32% 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

11 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Effects and molecular mechanisms ofFrontiers in pharmacology · 2025
    Review
  5. Review
  6. Review
  7. Article
  8. Extracellular histones induce inflammation and senescence of vascular smooth muscle cells by activating the AMPK/FOXO4 signaling pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Article
  9. 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

5 authors at 1 institution in 1 country.

Chongwei ZhengDepartment of Emergency and Critical Care Medicine, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences Guangzhou 510080, Guangdong, China.
Dongxin LiDepartment of Emergency and Critical Care Medicine, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences Guangzhou 510080, Guangdong, China.
Weifeng ZhanDepartment of Emergency and Critical Care Medicine, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences Guangzhou 510080, Guangdong, China.
Kairan HeDepartment of Emergency and Critical Care Medicine, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences Guangzhou 510080, Guangdong, China.
Hang YangDepartment of Emergency and Critical Care Medicine, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences Guangzhou 510080, Guangdong, China.
Guangdong Academy of Medical Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophages participate in all stages of sepsis and affect immune homeostasis and inflammatory processes. Small ubiquitin-like modifier (SUMO) protease SENP1 plays an important role in cellular inflammation by regulating proteins in SUMOylation. However, the roles and related mechanisms of SENP1 in macrophage inflammation during sepsis are largely unknown. In the present study, SENP1 expression was significantly promoted in lipopolysaccharide (LPS)-induced RAW 264.7 cells; furthermore, the knock down of SENP1 reduced the expression of inflammatory cytokines interleukin-6 and tumor necrosis factor-α. Momordin Ic (MC), a new type of SENP1 inhibitor, reduces LPS-induced cellular inflammation by depressing SENP1 expression. Moreover, the effect of SENP1 on LPS-induced inflammatory response was dependent on SENP1-Sp3 interaction and the promotion of Sp3 expression via Sp3 deSUMOylation. Furthermore, MC-depressed Sp3 expression disturbed Sp3-nuclear factor (NF)-κB interaction and then alleviated LPS-induced cellular inflammation. These results suggest that SENP1 promotes LPS-induced macrophage inflammation by promoting Sp3 expression via deSUMOylation and Sp3-NF-κB interaction in sepsis.

Indexed as

inflammationmacrophageSENP1sepsisSp3

Identifiers

PMID33312380
PMCPMC7724363
OpenAlexW3117082504

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.