Evidence map›Paper›PMID 40642004›Full record

ReviewFrontiers in pharmacology2025

Oxidative stress in ARDS: mechanisms and therapeutic potential.

Fengyun Wang, Ruiqi Ge, Yun Cai, Mingrui Zhao, Zhen Fang, Jingguo Li, Chengzhi Xie, Mei Wang, Wanyue Li, Xiaozhi Wang

Abstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing 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

25 citing papers in PubMed.

  1. Review
  2. Article
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  7. Review
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  11. Article
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  14. 4-Hydroxynonenal, a Potential Biomarker for Lung Inflammatory Diseases.International journal of molecular sciences · 2026
    Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Lipoxin A4 AttenuatesJournal of inflammation research · 2026
    Article
  20. 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

10 authors.

Fengyun Wang *Department of Critical Care Medicine, Second Affiliated Hospital of Hainan Medical University, Haikou, China.
Ruiqi Ge *Department of Critical Care Medicine, Zhongnan Hospital, Wuhan University, Wuhan, Hubei, China.
Yun CaiDepartment of Critical Care Medicine, Second Affiliated Hospital of Hainan Medical University, Haikou, China.
Mingrui ZhaoDepartment of Critical Care Medicine, Second Affiliated Hospital of Hainan Medical University, Haikou, China.
Zhen FangDepartment of Critical Care Medicine, Second Affiliated Hospital of Hainan Medical University, Haikou, China.
Jingguo LiDepartment of Critical Care Medicine, Second Affiliated Hospital of Hainan Medical University, Haikou, China.
Chengzhi XieDepartment of Critical Care Medicine, Second Affiliated Hospital of Hainan Medical University, Haikou, China.
Mei WangDepartment of Critical Care Medicine, Second Affiliated Hospital of Hainan Medical University, Haikou, China.
Wanyue LiDepartment of Critical Care Medicine, Second Affiliated Hospital of Hainan Medical University, Haikou, China.
Xiaozhi WangDepartment of Critical Care Medicine, Second Affiliated Hospital of Hainan Medical University, Haikou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute respiratory distress syndrome (ARDS) is a life-threatening condition characterized by acute lung inflammation, increased vascular permeability, and hypoxemic respiratory failure. Oxidative stress, driven by excessive reactive oxygen species (ROS), is a key contributor to ARDS pathogenesis, causing cellular damage, inflammation, and alveolar-capillary barrier disruption. This review elucidates the mechanisms of oxidative stress in ARDS, focusing on ROS production via NADPH oxidase (NOX) and mitochondria, which activate pathways like NF-κB and MAPK, promoting pro-inflammatory cytokine release. ROS-induced lipid and protein peroxidation, endothelial dysfunction, and programmed cell death (PCD), including apoptosis, pyroptosis, and ferroptosis, exacerbate lung injury. In COVID-19-related ARDS, SARS-CoV-2 spike protein amplifies mitochondrial ROS, worsening outcomes. Antioxidant therapies falter due to non-specific ROS suppression, patient heterogeneity (e.g., GSTP1 polymorphisms), and poor bioavailability. We propose a model where oxidative stress drives ARDS stages-early alveolar injury and late systemic dysfunction-suggesting targeted therapies like endothelial-specific nanoparticles or ferroptosis inhibitors. Precision medicine using biomarkers (e.g., mtDNA) and gender-specific approaches (e.g., estrogen-Nrf2 regulation) could enhance outcomes. This review bridges mechanistic gaps, critiques therapeutic failures, and advocates novel strategies like mitochondrial-targeted therapies to improve ARDS management.

Indexed as

acute lung injury (ALI)acute respiratory distress syndrome (ARDS)inflammationoxidative stressreactive oxygen species (ROS)

Identifiers

PMID40642004
PMCPMC12241040

What OpenQuestion holds

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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.