ArticleActa cirurgica brasileira2026
The role of TIPE2 in hemorrhagic shock-induced acute lung injury.
Article in Acta cirurgica brasileira, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeAcute lung injury is the most severe complication of hemorrhagic shock and closely correlates with the mortality rate of hemorrhagic shock. TIPE2 is a critical regulator of inflammation and is implicated in the pathogenesis of various inflammatory diseases. However, its role in hemorrhagic shock-induced acute lung injury is unclear, and the underlying mechanisms remain to be elucidated. Therefore, the purpose of this study was to investigate the role of TIPE2 in hemorrhagic shock-induced acute lung injury and its underlying mechanisms.
methodsC57BL/6J and TIPE2 knockout mice were used to establish hemorrhagic shock model, with a sham surgery as the control. The pulmonary ventilation function was evaluated using in-vivo testing system. Blood gas analysis was conducted to evaluate changes in blood oxygen level, reflecting the body's acid-base balance. Hematoxylin and eosin staining facilitated the observation of lesion progression in pulmonary tissue. The expression levels of TIPE2, myeloperoxidase, and citrullinated histone in lung tissues were determined by Western blotting, whereas the levels of tumor necrosis factor-α and IFN-γ in bronchoalveolar lavage fluid were quantified by enzyme-linked immunosorbent assay to evaluate the levels of key inflammatory mediators. VE-cadherin and E-cadherin expression in lung tissues were assessed by Western blotting to indicate changes of lung microvascular and alveolar permeability.
resultsFollowing hemorrhagic shock, mice developed severe acute lung injury, characterized by impaired lung function, respiratory acidosis, structural damage, and pulmonary edema. This was accompanied by a heightened inflammatory response, evidenced by elevated neutrophil activity and pro-inflammatory cytokines, alongside impaired endothelial and epithelial barrier integrity. Notably, TIPE2 knockout conferred protection against hemorrhagic shock-induced lung injury in mice.
conclusionTIPE2 knockout attenuates hemorrhagic shock-induced acute lung injury through mechanisms involving downregulation of inflammatory-associated protein expression, suppression of proinflammatory cytokine release, and restoration of pulmonary barrier permeability.
Indexed as
Identifiers
What Socratic holds
Registered trials
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 Socratic graph.