Evidence map›Paper›PMID 41192752›Full record

ArticleMetabolism: clinical and experimental2026

Hepatic steatosis associates with leukopoietic activity and atherosclerotic inflammation: mechanistic insights into cardiovascular risk.

Shady Abohashem, Wesam Aldosoky, Taimur Abbasi, Tawseef Dar, Robert Rollings, Brian Tung, Basma Hammad, Fatima Saeed, Abdelrahman Ali, Richard A P Takx and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Metabolism: clinical and experimental, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
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.

Shady AbohashemCardiovascular Imaging Research Center, Radiology Department, Massachusetts General Hospital, Harvard Medical School, Boston, USA; Cardiology Department, Massachusetts General Hospital, Harvard Medical School, Boston, USA. Electronic address: SAbohashem@mgh.harvard.edu.
Wesam AldosokyCardiovascular Imaging Research Center, Radiology Department, Massachusetts General Hospital, Harvard Medical School, Boston, USA.
Taimur AbbasiDepartment of Internal Medicine, Rush University Medical Center, Chicago, USA.
Tawseef DarCardiology Department, Mount Sinai Medical Center, NYC, USA.
Robert RollingsCardiovascular Imaging Research Center, Radiology Department, Massachusetts General Hospital, Harvard Medical School, Boston, USA.
Brian TungRadiology Department, Westchester Medical Center, NYC, USA.
Basma HammadCardiology Department, Alexandria University, Alexandria, Egypt.
Fatima SaeedCardiovascular Imaging Research Center, Radiology Department, Massachusetts General Hospital, Harvard Medical School, Boston, USA.
Abdelrahman AliCardio-oncology Department, MD Anderson Cancer Center, Houston, USA.
Richard A P TakxRadiology Department, Amsterdam University Medical Center, Amsterdam, Netherlands.
Brian B GhoshhajraCardiovascular Imaging Research Center, Radiology Department, Massachusetts General Hospital, Harvard Medical School, Boston, USA.
Ahmed TawakolCardiovascular Imaging Research Center, Radiology Department, Massachusetts General Hospital, Harvard Medical School, Boston, USA; Cardiology Department, Massachusetts General Hospital, Harvard Medical School, Boston, USA.
Michael T OsborneCardiovascular Imaging Research Center, Radiology Department, Massachusetts General Hospital, Harvard Medical School, Boston, USA; Cardiology Department, Massachusetts General Hospital, Harvard Medical School, Boston, USA.

Funding

ROLE OF DIETARY CONSTITUENTS ON GENE EXPRESSION IN INTESTINAL EPITHELIUMP30DK040561 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI Elizabeth Austen Lawson, Takara Leah Stanley · 1994 to 2026
$31.6M
The Effect of Mindfulness on Vascular Inflammation in Stable Coronary Disease: A Multi-System PET/MRI StudyK23HL151909 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI OSBORNE, MICHAEL THOMAS · 2021 to 2025
$997k
American Heart Association (AHA) 24SCEFIA1256969NHLBI NIH HHS K23 HL151909NIDDK NIH HHS P30 DK040561
6 · The paper itself

Abstract

backgroundHepatic steatosis (HS) is associated with an increased risk of major adverse cardiovascular events (MACE). However, the underlying mechanisms linking HS to MACE remain incompletely understood. This study aimed to investigate the role of the leukopoietic-arterial axis in mediating the relationship between imaging markers of HS and MACE. METHODS AND MATERIALS: This longitudinal retrospective cohort study included 445 individuals without active cancer, liver disease or alcohol abuse, or baseline cardiovascular disease who underwent clinical

resultsIn fully adjusted models, HGU associated with heightened BM (standardized β [95 % confidence interval]: 0.353 [0.276, 0.430], p < 0.001) and spleen activities (0.548 [0.475, 0.621], p < 0.001) as well as ArtI (0.529 [0.453, 0.605], p < 0.001). Similar associations were observed for HAI and MASLD or NAFLD status. Notably, these associations remained significant after adjusting for other confounders and among individuals without MASLD/NAFLD. A total of 28 individuals developed MACE over 4 years median follow-up. Furthermore, the leukopoietic-arterial activity mediated the link between imaging markers of HS (i.e., HGU, HAI, MASLD) and MACE, (p < 0.05).

conclusionOur study suggests an important role for the leukopoietic-arterial axis in HS and MACE. These findings may inform therapeutic avenues for reducing the cardiovascular risk associated with HS. STRUCTURED ABSTRACT: This study examines the connection between hepatic steatosis (HS) and major adverse cardiovascular events (MACE) through the leukopoietic-arterial axis. Among 445 patients without history of liver disease or alcohol abuse, imaging markers of hepatic steatosis (i.e., hepatic glucose uptake (HGU)), and metabolic dysfunction associated steatotic liver disease (MASLD), associated with increased activity in bone marrow and spleen, and atherosclerotic plaques. These associations persisted irrespective of MASLD status and after adjusting for relevant confounders. Heightened uptake in leukopoietic tissues and the arteries mediated the relationship between HS markers (i.e., HGU, MASLD) and MACE development. These findings shed light on novel mechanistic pathways and potential targets for interventions to reduce the burden of HS-related CVD.

Indexed as

AtherosclerosisCardiovascular DiseasesFatty LiverHematopoiesisInflammationAdultAgedBone MarrowFemaleFluorodeoxyglucose F18Heart Disease Risk FactorsHumansLiverLongitudinal StudiesMaleMiddle AgedFluorodeoxyglucose F18Arterial inflammationHepatic steatosisLeukopoietic-arterial axisMajor adverse cardiovascular eventsMediationMetabolic dysfunction associated steatotic liver diseaseNon-alcoholic fatty liver disease

Identifiers

PMID41192752
PMCPMC13047517

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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 OpenQuestion graph.