Evidence map›Paper›PMID 40584894›Full record

ArticleFrontiers in molecular biosciences2025

Hyperbaric oxygen pretreatment on endothelial cell injury via heat shock factor 1 in decompression sickness.

Caiyi Xu, Quan Zhou, Xiangyang Meng, Jiahe Zhou, Xuhua Yu, Juan Zheng, Hongjie Yi, Guoyang Huang, Weigang Xu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in molecular biosciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. 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

9 authors.

Caiyi Xu *Naval Medical Center, Naval Medical University, Shanghai, China.
Quan Zhou *Naval Medical Center, Naval Medical University, Shanghai, China.
Xiangyang MengNaval Medical Center, Naval Medical University, Shanghai, China.
Jiahe ZhouNaval Medical Center, Naval Medical University, Shanghai, China.
Xuhua YuNaval Medical Center, Naval Medical University, Shanghai, China.
Juan ZhengNaval Medical Center, Naval Medical University, Shanghai, China.
Hongjie YiNaval Medical Center, Naval Medical University, Shanghai, China.
Guoyang HuangNaval Medical Center, Naval Medical University, Shanghai, China.
Weigang XuNaval Medical Center, Naval Medical University, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: This study investigated the protective role and mechanisms of hyperbaric oxygen (HBO) pretreatment in enhancing vascular endothelial cell (VEC) resistance to bubble-induced injury by focusing on heat shock factor 1 (HSF-1) to prevent decompression sickness (DCS). Methods: Primary cultured rat pulmonary microvascular endothelial cells (PMVECs) and Sprague-Dawley rats were used as experimental models. Western blot analysis was performed to examine the activation patterns of HSF-1 and the expression of downstream proteins after HBO exposure. Specific inhibitors were used to delineate the signaling pathways involved in HSF-1 activation. At peak protein expression time points, a cellular bubble-induced injury model and a rat DCS model were established. The functional roles of HSF-1 and its downstream proteins in protection against HBO were evaluated using specific inhibitors and siRNAs. Results: HBO significantly enhanced the nuclear translocation of HSF-1 and upregulated the expression of downstream heat shock proteins 27 and 40 in PMVECs and lung tissues, peaking at 12 and 18 h after HBO exposure, respectively. The reactive oxygen species (ROS) levels and phosphorylation of ERK1/2, P38 MAPK, and AKT were markedly elevated after HBO exposure. AKT inhibition substantially suppressed HSF-1 activation, whereas ERK1/2 and P38 MAPK inhibition had no effect. ROS scavenging with Mito-Tempo reduced AKT phosphorylation and HSF-1 activation. Bubble-induced injury significantly decreased the viability of PMVECs and increased the levels of endothelial microparticles, inflammatory cytokines, and endothelial injury markers in culture media. HBO pretreatment ameliorated these pathological changes, which were reversed by HSF-1, HSP27, or HSP40 inhibition. In DCS rats, HBO pretreatment decreased lung wet-to-dry ratios, histopathological scores, serum inflammatory cytokines, endothelial microparticles, and endothelial injury markers. These benefits were reversed by the HSF-1 inhibitor KRIBB11. Conclusion: HBO pretreatment enhanced VEC resistance to bubble injury and mitigated DCS-related damage in rats via HSP27 and HSP40 expression upregulated by the ROS/AKT/HSF-1 signaling pathway.

Indexed as

decompression sicknessheat shock factor 1hyperbaric oxygenprotective proteinpulmonary microvascular endothelial cells

Identifiers

PMID40584894
PMCPMC12202230

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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.