Evidence map›Paper›PMID 38218783›Full record

ReviewRespiratory research2024

Signaling pathways and potential therapeutic targets in acute respiratory distress syndrome (ARDS).

Qianrui Huang, Yue Le, Shusheng Li, Yi Bian

Open access · goldAbstract readReview
In one paragraph

Review in Respiratory research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
28.1field-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

66 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
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  8. Alternative splicing of toll-like receptor pathway mRNAs in lung immune cells from patients with ARDS.American journal of physiology. Lung cellular and molecular physiology · 2026
    Article
  9. Review
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  17. The Lectin fromInternational journal of molecular sciences · 2026
    Article
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  20. Review

6 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

4 authors at 2 institutions in 1 country.

Qianrui Huang *Department of Critical Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, No.1095, Jie Fang Avenue, Wuhan, 430030, China.
Yue Le *Department of Critical Care Medicine, Zhongda Hospital, School of Medicine, Southeast University, 87 Dingjia Bridge, Hunan Road, Gu Lou District, Nanjing, 210009, China.
Shusheng LiDepartment of Critical Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, No.1095, Jie Fang Avenue, Wuhan, 430030, China. lishusheng@hust.edu.cn.
Yi BianDepartment of Critical Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, No.1095, Jie Fang Avenue, Wuhan, 430030, China. bianyi2526@163.com.
Huazhong University of Science and Technology · CNZhongda Hospital Southeast University · CN

Funding

China Primary Health Care Foundation No. YLGX-ZZ-2020001Natural Science Foundation of Hubei Province No. 2021CFB376
6 · The paper itself

Abstract

Acute respiratory distress syndrome (ARDS) is a common condition associated with critically ill patients, characterized by bilateral chest radiographical opacities with refractory hypoxemia due to noncardiogenic pulmonary edema. Despite significant advances, the mortality of ARDS remains unacceptably high, and there are still no effective targeted pharmacotherapeutic agents. With the outbreak of coronavirus disease 19 worldwide, the mortality of ARDS has increased correspondingly. Comprehending the pathophysiology and the underlying molecular mechanisms of ARDS may thus be essential to developing effective therapeutic strategies and reducing mortality. To facilitate further understanding of its pathogenesis and exploring novel therapeutics, this review provides comprehensive information of ARDS from pathophysiology to molecular mechanisms and presents targeted therapeutics. We first describe the pathogenesis and pathophysiology of ARDS that involve dysregulated inflammation, alveolar-capillary barrier dysfunction, impaired alveolar fluid clearance and oxidative stress. Next, we summarize the molecular mechanisms and signaling pathways related to the above four aspects of ARDS pathophysiology, along with the latest research progress. Finally, we discuss the emerging therapeutic strategies that show exciting promise in ARDS, including several pharmacologic therapies, microRNA-based therapies and mesenchymal stromal cell therapies, highlighting the pathophysiological basis and the influences on signal transduction pathways for their use.

Indexed as

MicroRNAsPulmonary EdemaRespiratory Distress SyndromeHumansLungSignal TransductionMicroRNAsAcute respiratory distress syndromePathogenesisPathophysiologySignaling pathwaysTherapeutics

Identifiers

PMID38218783
PMCPMC10788036
OpenAlexW4390838116

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.