Evidence map›Paper›PMID 41023070›Full record

ArticleScientific reports2025

Plasma apolipoprotein A-I is a causal protective factor in sepsis.

Kyle R Campbell, Kantimas Sitthikool, Kelly Roveran Genga, Nozomi Takahashi, Peiyuan Zhu, Tadanaga Shimada, Taka-Aki Nakada, John H Boyd, James A Russell, Keith R Walley

Erratum issuedAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. 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

5 · Who and what money

Authors and funding

10 authors.

Kyle R CampbellCentre for Heart Lung Innovation, St. Paul's Hospital, The University of British Columbia, 1081 Burrard Street, Vancouver, BC, V6Z 1Y6, Canada.
Kantimas SitthikoolCentre for Heart Lung Innovation, St. Paul's Hospital, The University of British Columbia, 1081 Burrard Street, Vancouver, BC, V6Z 1Y6, Canada.
Kelly Roveran GengaCentre for Heart Lung Innovation, St. Paul's Hospital, The University of British Columbia, 1081 Burrard Street, Vancouver, BC, V6Z 1Y6, Canada.
Nozomi TakahashiCentre for Heart Lung Innovation, St. Paul's Hospital, The University of British Columbia, 1081 Burrard Street, Vancouver, BC, V6Z 1Y6, Canada.
Peiyuan ZhuCentre for Heart Lung Innovation, St. Paul's Hospital, The University of British Columbia, 1081 Burrard Street, Vancouver, BC, V6Z 1Y6, Canada.
Tadanaga ShimadaDepartment of Emergency and Critical Care Medicine, Chiba University Graduate School of Medicine, Chiba, Japan.
Taka-Aki NakadaDepartment of Emergency and Critical Care Medicine, Chiba University Graduate School of Medicine, Chiba, Japan.
John H BoydCentre for Heart Lung Innovation, St. Paul's Hospital, The University of British Columbia, 1081 Burrard Street, Vancouver, BC, V6Z 1Y6, Canada.
James A RussellCentre for Heart Lung Innovation, St. Paul's Hospital, The University of British Columbia, 1081 Burrard Street, Vancouver, BC, V6Z 1Y6, Canada.
Keith R WalleyCentre for Heart Lung Innovation, St. Paul's Hospital, The University of British Columbia, 1081 Burrard Street, Vancouver, BC, V6Z 1Y6, Canada. Keith.Walley@hli.ubc.ca.

Funding

CIHR FDN154311
6 · The paper itself

Abstract

Apolipoprotein AI (ApoAI), the main component of high-density lipoprotein (HDL), binds pathogen lipids to limit inflammation. We performed a retrospective analysis of 442,601 European patients in the UK Biobank (UKB) cohort focused on sepsis patients (n = 11,643). We tested for a causal contribution of ApoAI using Mendelian randomization with an ApoAI genetic score as an instrumental variable, with sensitivity analyses to control for genetic confounders and instrumental variable assumptions. Sensitivity analyses controlled for confounders, and validation was performed in transancestry sepsis cohorts VASST (Europeans, n = 632) and Chiba (East Asians, n = 536). Median baseline ApoAI levels were lower in individuals who later developed sepsis (1.45 g/L) than in those who did not (1.51 g/L; P < 0.0001). Mendelian randomization in UKB showed ApoAI as protective against sepsis incidence (OR = 0.87, 95%CI [0.86,0.89], P = 7.4 × 10

Indexed as

Apolipoprotein A-ISepsisAgedFemaleHumansMaleMendelian Randomization AnalysisMiddle AgedProtective FactorsRetrospective StudiesUnited KingdomAPOA1 protein, humanApolipoprotein A-IApolipoprotein A-ICausalityHigh density lipoproteinLipopolysaccharidesSepsis

Identifiers

PMID41023070
PMCPMC12480524

What OpenQuestion holds

Textmetadata
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.