Evidence map›Paper›PMID 36982166›Full record

ArticleInternational journal of molecular sciences2023

Uridine Alleviates Sepsis-Induced Acute Lung Injury by Inhibiting Ferroptosis of Macrophage.

Kai Lai, Congkuan Song, Minglang Gao, Yu Deng, Zilong Lu, Ning Li, Qing Geng

Open access · goldFull text read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
36.4field-weighted citation impact, top 1% 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

79 citing papers in PubMed, 137 citations in OpenAlex.

  1. Article
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  9. Article
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19 more citing papers are in PubMed but not listed here.

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

7 authors at 1 institution in 1 country.

Kai LaiDepartment of Thoracic Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Congkuan SongDepartment of Thoracic Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Minglang GaoDepartment of Thoracic Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Yu DengDepartment of Thoracic Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Zilong LuDepartment of Thoracic Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Ning LiDepartment of Thoracic Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Qing GengDepartment of Thoracic Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, China.ORCID 0000-0003-4515-5084
Wuhan University · CN

Funding

National Natural Science Foundation of China 81770095Natural Science Foundation of Hubei Province 2020CFA027
6 · The paper itself

Abstract

Uridine metabolism is extensively reported to be involved in combating oxidative stress. Redox-imbalance-mediated ferroptosis plays a pivotal role in sepsis-induced acute lung injury (ALI). This study aims to explore the role of uridine metabolism in sepsis-induced ALI and the regulatory mechanism of uridine in ferroptosis. The Gene Expression Omnibus (GEO) datasets including lung tissues in lipopolysaccharides (LPS) -induced ALI model or human blood sample of sepsis were collected. In vivo and vitro, LPS was injected into mice or administered to THP-1 cells to generate sepsis or inflammatory models. We identified that uridine phosphorylase 1 (UPP1) was upregulated in lung tissues and septic blood samples and uridine significantly alleviated lung injury, inflammation, tissue iron level and lipid peroxidation. Nonetheless, the expression of ferroptosis biomarkers, including SLC7A11, GPX4 and HO-1, were upregulated, while lipid synthesis gene (ACSL4) expression was greatly restricted by uridine supplementation. Moreover, pretreatment of ferroptosis inducer (Erastin or Era) weakened while inhibitor (Ferrostatin-1 or Fer-1) strengthened the protective effects of uridine. Mechanistically, uridine inhibited macrophage ferroptosis by activating Nrf2 signaling pathway. In conclusion, uridine metabolism dysregulation is a novel accelerator for sepsis-induced ALI and uridine supplementation may offer a potential avenue for ameliorating sepsis-induced ALI by suppressing ferroptosis.

Indexed as

Acute Lung InjuryFerroptosisSepsisAnimalsHumansLipopolysaccharidesMacrophagesMiceNF-E2-Related Factor 2LipopolysaccharidesNF-E2-Related Factor 2acute lung injuryferroptosismacrophageoxidative stressuridine

Identifiers

PMID36982166
PMCPMC10049139
OpenAlexW4323566544

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Registered trials

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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.