Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ACBP: a poor-prognosis biomarker in sepsis and a target for disease mitigation [Lung]

ABSTRACT: Sepsis remains a major clinical challenge, with high mortality and long-term disability despite current interventions. Here, we identify the tissue hormone acyl-CoA–binding protein (ACBP), also known as diazepam-binding inhibitor (DBI), as a biomarker and driver of poor outcome in sepsis. ACBP/DBI was elevated in the plasma of septic patients and associated with organ dysfunction and increased mortality. In murine models of endotoxemia, Escherichia coli infection, and polymicrobial sepsis, genetic deletion or antibody-mediated neutralization of ACBP/DBI conferred robust protection by enhancing pathogen clearance, dampening cytokine storm, and preserving organ function. Notably, ACBP/DBI inhibition could be favorably combined with glucocorticoids, enhancing survival and reversing histopathological, transcriptional, or metabolic signatures of septic shock across heart, kidney, liver, lung, spleen, and plasma. These findings position ACBP/DBI as a mechanistic amplifier of sepsis pathophysiology and propose its neutralization, alone or in combination with corticosteroids, as a promising therapeutic strategy to interrupt the fatal trajectory of septic shock.

ORGANISM(S): Mus musculus

PROVIDER: GSE313149 | GEO | 2026/01/26

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

ACBP: a poor-prognosis biomarker in sepsis and a target for disease mitigation

Project description:Septic shock remains a major clinical challenge, with high mortality and long-term disability despite current interventions. Here, we identify the tissue hormone acyl-CoA–binding protein (ACBP), also known as diazepam-binding inhibitor (DBI), as a biomarker and driver of poor outcomes in sepsis. ACBP/DBI was elevated in the plasma of septic patients, correlating with organ dysfunction and mortality. In murine models of endotoxemia, Escherichia coli infection, and polymicrobial sepsis, genetic deletion or antibody-mediated neutralization of ACBP/DBI conferred robust protection by enhancing pathogen clearance, dampening cytokine storms, and preserving organ function. Notably, ACBP/DBI inhibition could be favorably combined with glucocorticoids, enhancing survival and reversing transcriptional and metabolic signatures of septic shock across spleen, liver, heart, and kidney. These findings position ACBP/DBI as a mechanistic amplifier of sepsis pathophysiology and propose its neutralization—alone or combined with corticosteroids—as a promising therapeutic strategy to interrupt the fatal trajectory of septic shock.

2026-01-26 | GSE304860 | GEO

ACBP: a poor-prognosis biomarker in sepsis and a target for disease mitigation II

2026-01-26 | GSE304861 | GEO

Implication of Acyl Coenzyme A Binding Protein (ACBP) in Cushing Syndrome

Project description:Acyl coenzyme A binding protein (ACBP), encoded by the diazepam binding protein (DBI) gene, plays a pivotal role in stimulating appetite and lipo-anabolic reactions, showing correlations with laboratory indications of metabolic syndrome in ostensibly healthy individuals. In a screening effort targeting inhibitors of ACBP/DBI expression among distinct neuroendocrine factors, we discovered that glucocorticoids induce ACBP/DBI secretion in cultured cells. In mouse models of iatrogenic Cushing syndrome, antibody-mediated neutralization of ACBP/DBI prevented the metabolic consequences of prolonged glucocorticoid administration. Our findings suggest that a surge in extracellular ACBP/DBI may mediate crucial aspects of Cushing syndrome.

2024-10-02 | GSE248672 | GEO

Charaterization of potential roles and mechanisms of ACBP/DBI in NASH/MASH-dirven HCC mouse models

Project description:We demonstrated that ACBP/DBI inhibition impaired hepatocarcinogenesis in NASH/MASH-driven HCC models. To further investigate its potential mechanisms at transcriptional level in NASH/MASH-driven HCC models, we performed Bulk RNA-seq analyses with liver tissues from the following three models, namely, (i) WD/CCl4 with tamoxifen inducible ACBP/DBI knout mice (Dbi-/- mice, Dbi+/+ mice as control) for in total 27 weeks; (ii) WD/CCl4 with KLH/KLH-ACBP immunized mice for in total 34 weeks; and (iii) HFD/DEN with KLH/KLH-ACBP immunized miceI for a total of 36 weeks.

2025-04-18 | GSE255799 | GEO

Supplementation of ACBP/DBI for the Experimental Treatment of Anorexia Nervosa

Project description:Total liver RNA extracts from adult female mice (8-week-old) subjected to CRS (chronic restraint stress) or CDDP (cisplatin) induced anorexia with or without ACBP/DBI delivery to investigate the impact of ACBP/DBI on anorexia-induced transcriptomic alterations.

2024-07-12 | GSE237766 | GEO

ACBP/DBI protein neutralization for the experimental treatment of fatty liver disease

Project description:Total liver RNA extracts from adult male mice (8 weeks old, C57BL/6) subjected to Methionine and Choline Deficient Diet (regime duration: 6 weeks) and injected with monoclonal anti-ACBP/DBI (2 doses per week from week 4) were determinated to describe the therapeutic effects of neutrali-zation of ACBP/DBI to MASH-induced transcriptomic alterations.

2025-03-19 | GSE278209 | GEO

Neutralization of Acyl-CoA Binding Protein Confers Autophagy-Dependent Organ Protection

Project description:Total liver RNA extracts from adult male mice (8 weeks old, C57BL/6) injected with monoclonal anti-ACBP/DBI (1 dose per week) and subjected to Methionine and Choline Deficient Diet (regime duration: 4weeks) were analyzed to describe the effect of neutralization of ACBP/DBI to NASH-induced transcriptomic alterations.

2023-02-24 | GSE194346 | GEO

Spatial transcriptomic profiling of gene expression alterations following ACBP/DBI inhibition in a MASH-Driven HCC mouse model

Project description:We identified ACBP/DBI as a critical regulator in the pathogenesis of hepatocellular carcinoma (HCC), with its inhibition significantly impairing hepatocarcinogenesis in MASH-driven HCC models. To further elucidate the underlying transcriptional mechanisms, we performed spatial transcriptomic analyses using formalin-fixed, paraffin-embedded (FFPE) liver tissues from the following two experimental models: (i) Western diet (WD) and CCl₄-treated mice with tamoxifen-inducible ACBP/DBI knockout (Dbi⁻/⁻ mice), with Dbi⁺/⁺ littermates serving as controls, after a total of 27 weeks; (ii) WD and CCl₄-treated mice immunized with either keyhole limpet hemocyanin (KLH) alone or KLH-ACBP conjugate, after a total of 34 weeks.

2025-07-18 | GSE296545 | GEO

ACBP/DBI protein neutralization for the experimental treatment of fatty liver disease

Project description:ACBP/DBI protein neutralization for the experimental treatment of fatty liver disease

| PRJNA1166092 | ENA

Acyl-coA Binding Protein neutralization improves cancer immunosurveillance

Project description:The plasma concentrations of acyl coenzyme A binding protein (ACBP, also known as diazepam-binding inhibitor, DBI, or ‘endozepine’) increase with age and obesity, two parameters that are also the most important risk factors for cancer. In mice bearing MCA205 fibrosarcoma, antibody mediated ACBP/DBI neutralization enhanced the anticancer T-cell response in the context of chemoimmunotherapy. T-cells infiltrating MCA205 tumors were sorted and submitting to single-cell TCR sequencing and single-cell RNA sequencing (scRNAseq) to identify the mechanisms driving this improvement.

2024-09-11 | GSE242119 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data