Evidence map›Paper›PMID 33009637›Full record

ArticleInflammation2021

GPR120 Ameliorates Apoptosis and Inhibits the Production of Inflammatory Cytokines in Renal Tubular Epithelial Cells.

Deyuan Zhi, Meng Zhang, Jin Lin, Pei Liu, Meili Duan

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Supplementation with GPR120 (Ffar4) ligand omega-3 does not improve survival in murine sepsis models.American journal of physiology. Endocrinology and metabolism · 2025
    Article
  5. Oligomeric proanthocyanidin ameliorates sepsis-associated renal tubular injury: involvement of oxidative stress, inflammation, PI3K/AKT and NFκB signaling pathways.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Article
  6. Article
  7. Article
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  9. Article
  10. Review
  11. Article
  12. 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

5 authors at 1 institution in 1 country.

Deyuan ZhiDepartment of Critical Care Medicine, Beijing Friendship Hospital, Capital Medical University, No. 95 Yong'an Road, Xicheng District, Beijing, 100050, China.
Meng ZhangDepartment of Critical Care Medicine, Beijing Friendship Hospital, Capital Medical University, No. 95 Yong'an Road, Xicheng District, Beijing, 100050, China.
Jin LinDepartment of Critical Care Medicine, Beijing Friendship Hospital, Capital Medical University, No. 95 Yong'an Road, Xicheng District, Beijing, 100050, China.
Pei LiuDepartment of Critical Care Medicine, Beijing Friendship Hospital, Capital Medical University, No. 95 Yong'an Road, Xicheng District, Beijing, 100050, China.
Meili DuanDepartment of Critical Care Medicine, Beijing Friendship Hospital, Capital Medical University, No. 95 Yong'an Road, Xicheng District, Beijing, 100050, China. dmeili@bfh.com.cn.ORCID http://orcid.org/0000-0001-7871-5135
Capital Medical University · CN

Funding

Beijing Municipal Administration of Hospitals Clinical Medicine Development of Special Funding ZYLX201802
6 · The paper itself

Abstract

Acute kidney injury (AKI) is the most common complication of sepsis with a high mortality rate. In this study, we focus on the renal injury caused by the immune response of renal tubular epithelial cells and inflammation-induced renal tubular epithelial cell apoptosis. We studied the role of GRP120 in the inflammation and apoptosis of human renal cell line HK-2 and mouse primary renal tubular epithelial cells. GPR120 agonist GW9508 activated the GPR120 pathway. Inflammatory factors were detected using quantitative real-time PCR and enzyme-linked immunosorbent assay. Cell apoptosis experiments included the annexin V and PI double-staining method combined with flow cytometry, TUNEL method, and Western blot. The level of cytokines including TNF-α, IL-6, IL-1β, and iNOS was significantly decreased (P < 0.05) in HK-2 and TECs after the activation of the GPR120 pathway. Besides, the cell apoptosis of both cells increased. Overexpressed GPR120 and shGPR120 were established. Treatment with lipopolysaccharide (LPS) increased the level of cytokines including TNF-α, IL-6, IL-1β, and iNOS in HK-2 cell and TECs. Compared with control-LPS and negative control (NC)-LPS, the overexpression of GPR120 and shGPR120 could decrease and increase the level of secreted cytokines significantly (P < 0.05), respectively, after LPS-induced apoptosis. After H

Indexed as

Acute Kidney InjuryAnimalsApoptosisBiomarkersBlotting, WesternCell LineCytokinesEnzyme-Linked Immunosorbent AssayEpithelial CellsFlow CytometryHumansImmunity, CellularInflammationIn Situ Nick-End LabelingKidney TubulesMiceBiomarkersCytokinesFFAR4 protein, humanFFAR4 protein, mouseReceptors, G-Protein-Coupledacute kidney injuryapoptosisGPR120inflammationrenal tubular epithelial cells

Identifiers

PMID33009637
OpenAlexW3091425178

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.