Evidence map›Paper›PMID 41743980›Full record

ArticlebioRxiv : the preprint server for biology2026

ISG15 orchestrates dynamic crosstalk between mitochondrial fat oxidation and type 1 interferon in myeloid cells.

Anand Kumar Gupta, Jing Wu, Pijush Das, Rahul Sharma, Sonali Das, Kim Han, Rachael J Klein, Rebecca D Huffstutler, Christian Combs, Warren J Leonard and 3 more

Abstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 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

13 authors.

Anand Kumar GuptaLaboratory of Mitochondrial Biology and Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Jing WuLaboratory of Mitochondrial Biology and Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Pijush DasRadiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Rahul SharmaLaboratory of Mitochondrial Biology and Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Sonali DasLaboratory of Molecular Immunology, and the Immunology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Kim HanLaboratory of Mitochondrial Biology and Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Rachael J KleinLaboratory of Mitochondrial Biology and Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Rebecca D HuffstutlerCardiovascular Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Christian CombsLaboratory of Mitochondrial Biology and Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Warren J LeonardLaboratory of Molecular Immunology, and the Immunology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Claudia KemperLaboratory for Complement and Inflammation Research, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Erin E WestLaboratory for Complement and Inflammation Research, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Michael N SackLaboratory of Mitochondrial Biology and Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.ORCID 0000-0002-3411-0000

Funding

Mitochondrial Biology in Cardiovascular DiseaseZ01HL005102 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI SACK, MICHAEL · 2005 to 2008
$1.2M
Intramural NIH HHS Z01 HL005102
6 · The paper itself

Abstract

In contrast to Krebs cycle intermediates, the role of mitochondrial fatty acid oxidation (FAO) in immunometabolism remains incompletely characterized. Studying primary bone marrow-derived macrophages (BMDMs), we show that IFN-β and STING activation augments FAO and associated enzymes carnitine palmitoyltransferase 1a (CPT1a) and acetyl-CoA acetyltransferase 1 (ACAT1). Depleting BMDM

Indexed as

ACAT1BMDMsCPT1afatty acid oxidationISG15LCMVlupusmetabolismmyeloid cellstype I interferons

Identifiers

PMID41743980
PMCPMC12930444

What OpenQuestion holds

Textmetadata
LicenceCC0
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.