Evidence map›Paper›PMID 37350396›Full record

ArticleInternational journal of molecular medicine2023

Inflammation and coagulation abnormalities via the activation of the HMGB1‑RAGE/NF‑κB and F2/Rho pathways in lung injury induced by acute hypoxia.

Jing Gao, Zhuo Zhang, Jia-Yi Yan, Yun-Xuan Ge, Yue Gao

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2023. 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
3.1field-weighted citation impact, top 8% 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, 16 citations in OpenAlex.

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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.

Jing GaoDepartment of Pharmaceutical Sciences, Beijing Institute of Radiation Medicine, Beijing 100850, P.R. China.
Zhuo ZhangDepartment of Pharmaceutical Sciences, Beijing Institute of Radiation Medicine, Beijing 100850, P.R. China.
Jia-Yi YanDepartment of Pharmaceutical Sciences, Beijing Institute of Radiation Medicine, Beijing 100850, P.R. China.
Yun-Xuan GeDepartment of Pharmaceutical Sciences, Beijing Institute of Radiation Medicine, Beijing 100850, P.R. China.
Yue GaoDepartment of Pharmaceutical Sciences, Beijing Institute of Radiation Medicine, Beijing 100850, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High‑altitude acute hypoxia is commonly associated with respiratory cardiovascular diseases. The inability to adapt to acute hypoxia may lead to cardiovascular dysfunction, lung injury and even death. Therefore, understanding the molecular basis of the adaptation to high‑altitude acute hypoxia may reveal novel therapeutic approaches with which to counteract the detrimental consequences of hypoxia. In the present study, a high‑altitude environment was simulated in a rat model in order to investigate the role of the high mobility group protein‑1 (HMGB1)/receptor for advanced glycation end products (RAGE)/NF‑κB and F2/Rho signaling pathways in lung injury induced by acute hypoxia. It was found that acute hypoxia caused inflammation through the HMGB1/RAGE/NF‑κB pathway and coagulation dysfunction through the F2/Rho pathway, both of which may be key processes in acute hypoxia‑induced lung injury. The present study provides new insight into the molecular basis of lung injury induced by acute hypoxia. The simultaneous activation of the HMGB1/RAGE/NF‑κB and F2/Rho signaling pathways plays a critical role in hypoxia‑induced inflammatory responses and coagulation abnormalities, and provides a theoretical basis for the development of potential therapeutic strategies.

Indexed as

Acute Lung InjuryBlood Coagulation DisordersHMGB1 ProteinAnimalsHypoxiaInflammationNF-kappa BRatsReceptor for Advanced Glycation End ProductsHMGB1 ProteinNF-kappa BReceptor for Advanced Glycation End Productscoagulationhypoxiainflammationlung injurysignaling pathways

Identifiers

PMID37350396
PMCPMC10555482
OpenAlexW4381335747

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.