Evidence map›Paper›PMID 41810645›Full record

ArticleBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas2026

Disulfidptosis modification patterns are involved in the immune microenvironment regulation of septic acute respiratory distress syndrome.

Qian Zhang, Junke Ge

Abstract read
In one paragraph

Article in Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

2 authors.

Qian ZhangIntensive Care Unit, Shandong Provincial Third Hospital, Shandong University, Shandong, Jinan, China.ORCID http://orcid.org/0009-0009-1826-5377
Junke GeIntensive Care Unit, Shandong Provincial Third Hospital, Shandong University, Shandong, Jinan, China.ORCID http://orcid.org/0009-0006-8547-7650

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Disulfidptosis is a new form of programmed cell death. However, there is limited information available regarding the impact of disulfidptosis on septic acute respiratory distress syndrome (ARDS). The 16 disulfidptosis-related genes (DRGs) were collected from a previous study. Gene expression data of sepsis and septic ARDS samples were downloaded from the Gene Expression Omnibus database. The risk score model in septic ARDS was constructed based on the DRGs, followed by the investigation of immune microenvironment in septic ARDS patients. Furthermore, septic ARDS patients were divided into different subtypes based on disulfidptosis modification patterns, and their immune characteristics were investigated. Finally, the differentially expressed genes among different subtypes were identified, and a diagnostic model was constructed. The risk score model based on 6 DRGs was constructed to distinguish sepsis patients from septic ARDS patients, with good performance. The immune microenvironment in septic ARDS patients was slightly different from sepsis patients. Additionally, septic ARDS patients were divided into two subtypes based on DRGs. Finally, three diagnostic models based on 3 hub genes were constructed to classify the two subtypes in septic ARDS patients. Our findings indicated that disulfidptosis might play a role in the immune microenvironment of septic ARDS.

Indexed as

Cellular MicroenvironmentDisulfidptosisRespiratory Distress SyndromeSepsisGene Expression ProfilingHumans

Identifiers

PMID41810645
PMCPMC12971013

What Socratic 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 Socratic graph.