Evidence map›Paper›PMID 38037103›Full record

ReviewJournal of hematology & oncology2023

Reactive oxygen species (ROS) scavenging biomaterials for anti-inflammatory diseases: from mechanism to therapy.

Jiatong Liu, Xiaoyue Han, Tingyue Zhang, Keyue Tian, Zhaoping Li, Feng Luo

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

Review in Journal of hematology & oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 291 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
291citing papers in PubMed, 1 pooled it
53.8field-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

291 citing papers in PubMed, 1 synthesis or guideline pooled it, 491 citations in OpenAlex.

  1. Pooled it
  2. Article
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  6. Advancements in Functional Polymeric Scaffolds for Scar-Free Skin Regeneration.Polymer science & technology (Washington, D.C.) · 2026
    Review
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231 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

6 authors at 2 institutions in 1 country.

Jiatong Liu *State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China School of Stomatology, Sichuan University, Chengdu, 610041, China.
Xiaoyue Han *State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China School of Stomatology, Sichuan University, Chengdu, 610041, China.
Tingyue ZhangState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China School of Stomatology, Sichuan University, Chengdu, 610041, China.
Keyue TianState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China School of Stomatology, Sichuan University, Chengdu, 610041, China.
Zhaoping LiState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China School of Stomatology, Sichuan University, Chengdu, 610041, China.
Feng LuoState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China School of Stomatology, Sichuan University, Chengdu, 610041, China. luofeng0122@scu.edu.cn.
Sichuan University · CNState Key Laboratory of Oral Diseases

Funding

National Outstanding Youth Science Fund Project of National Natural Science Foundation of China 82001107the Applied Basic Research Project of Sichuan province 2022NSFSC1345
6 · The paper itself

Abstract

Inflammation is a fundamental defensive response to harmful stimuli, but the overactivation of inflammatory responses is associated with most human diseases. Reactive oxygen species (ROS) are a class of chemicals that are generated after the incomplete reduction of molecular oxygen. At moderate levels, ROS function as critical signaling molecules in the modulation of various physiological functions, including inflammatory responses. However, at excessive levels, ROS exert toxic effects and directly oxidize biological macromolecules, such as proteins, nucleic acids and lipids, further exacerbating the development of inflammatory responses and causing various inflammatory diseases. Therefore, designing and manufacturing biomaterials that scavenge ROS has emerged an important approach for restoring ROS homeostasis, limiting inflammatory responses and protecting the host against damage. This review systematically outlines the dynamic balance of ROS production and clearance under physiological conditions. We focus on the mechanisms by which ROS regulate cell signaling proteins and how these cell signaling proteins further affect inflammation. Furthermore, we discuss the use of potential and currently available-biomaterials that scavenge ROS, including agents that were engineered to reduce ROS levels by blocking ROS generation, directly chemically reacting with ROS, or catalytically accelerating ROS clearance, in the treatment of inflammatory diseases. Finally, we evaluate the challenges and prospects for the controlled production and material design of ROS scavenging biomaterials.

Indexed as

Biocompatible MaterialsOxidative StressAnti-Inflammatory AgentsHumansInflammationProteinsReactive Oxygen SpeciesAnti-Inflammatory AgentsBiocompatible MaterialsProteinsReactive Oxygen SpeciesAnti-inflammationBiomaterialsInflammatory diseaseReactive oxygen speciesSignaling pathways

Identifiers

PMID38037103
PMCPMC10687997
OpenAlexW4389201799

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.