Evidence map›Paper›PMID 40349771›Full record

ArticleMolecular metabolism2025

Functional regulation of macrophages by Ces1d-mediated lipid signaling in immunometabolism.

Long J Shao, Fathima Elizondo, Feng Gao, Rabie Habib, Xin Li, Katherine Pham, Jazmin Ysaguirre, Maryam Elizondo, Shirindokht Shirazi, Kristin L Eckel-Mahan and 3 more

Abstract read
In one paragraph

Article in Molecular metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Frontiers in microbiology · 2026
    Article
  9. Review
  10. 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.

Long J ShaoCenter for Metabolic and Degenerative Diseases, The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, University of Texas Health Science Center at Houston, Houston, TX, USA.
Fathima ElizondoCenter for Metabolic and Degenerative Diseases, The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, University of Texas Health Science Center at Houston, Houston, TX, USA.
Feng GaoDepartment of Medicine, Baylor College of Medicine, Houston, TX, USA.
Rabie HabibCenter for Metabolic and Degenerative Diseases, The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, University of Texas Health Science Center at Houston, Houston, TX, USA.
Xin LiCenter for Metabolic and Degenerative Diseases, The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, University of Texas Health Science Center at Houston, Houston, TX, USA.
Katherine PhamCenter for Metabolic and Degenerative Diseases, The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, University of Texas Health Science Center at Houston, Houston, TX, USA.
Jazmin YsaguirreCenter for Metabolic and Degenerative Diseases, The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, University of Texas Health Science Center at Houston, Houston, TX, USA.
Maryam ElizondoGraduate School of Biomedical Sciences (GSBS), University of Texas Health Science Center at Houston, Houston, TX, USA.
Shirindokht ShiraziCenter for Metabolic and Degenerative Diseases, The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, University of Texas Health Science Center at Houston, Houston, TX, USA; Graduate School of Biomedical Sciences (GSBS), University of Texas Health Science Center at Houston, Houston, TX, USA; Department of Epidemiology, School of Public Health, University of Texas Health Science Center at Houston, Houston, TX, USA.
Kristin L Eckel-MahanCenter for Metabolic and Degenerative Diseases, The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, University of Texas Health Science Center at Houston, Houston, TX, USA; Graduate School of Biomedical Sciences (GSBS), University of Texas Health Science Center at Houston, Houston, TX, USA.
Sean HartigDepartment of Medicine, Baylor College of Medicine, Houston, TX, USA.
Huaizhu WuDepartment of Medicine, Baylor College of Medicine, Houston, TX, USA.
Kai SunCenter for Metabolic and Degenerative Diseases, The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, University of Texas Health Science Center at Houston, Houston, TX, USA; Graduate School of Biomedical Sciences (GSBS), University of Texas Health Science Center at Houston, Houston, TX, USA. Electronic address: kai.sun@uth.tmc.edu.

Funding

METABOLIC IMPACTS OF TYPE II INTERFERON SIGNALS IN OBESITYR01DK114356 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI HARTIG, SEAN · 2017 to 2025
$4.6M
MICRORNA REGULATION OF ADIPOSE TISSUE IMMUNE RESPONSE IN OBESITYR01DK139397 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI Sean Hartig, Huaizhu Wu · 2024 to 2026
$2.0M
Inflammation and insulin resistance in agingR01AG065197 · NIA · BAYLOR COLLEGE OF MEDICINE · PI Huaizhu Wu · 2022 to 2026
$2.0M
Molecular regulation of leptin bioavailabilityR01DK138018 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI Sean Hartig · 2024 to 2026
$1.9M
Regulation of Type 1 Inflammation in Diet-induced ObesityR01DK121348 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI WU, HUAIZHU · 2020 to 2023
$1.6M
Discovering the new function of DRP1 on lipid metabolismR01DK129815 · NIDDK · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI SUN, KAI · 2022 to 2025
$1.5M
NIA NIH HHS R01 AG065197NIDDK NIH HHS R01 DK114356NIDDK NIH HHS R01 DK121348NIDDK NIH HHS R01 DK129815NIDDK NIH HHS R01 DK138018NIDDK NIH HHS R01 DK139397
6 · The paper itself

Abstract

objectiveMacrophage accumulation in metabolically active tissues during obesity is common in both animals and humans, but the lipid signaling mechanisms that trigger macrophage inflammation remain unclear. This study investigates the role of Ces1d, an unconventional lipase, in regulating macrophage inflammation under nutritional stress.

methodsA myeloid-specific Ces1d knockout (LysM-Cre-Ces1d

resultsCes1d expression changes during the differentiation of monocytes into macrophages in both mice and humans. Loss of Ces1d causes larger lipid droplets, with increased accumulation of triacylglycerol (TAG) and diacylglycerol (DAG), and impaired lipid signaling in KO macrophages. Lipid dysregulation in macrophages triggers pro-inflammatory activation, enhancing migration, activation, and polarization toward an M1-like phenotype. The pro-inflammatory macrophages further promote CD3+CD8+ T cell accumulation in obese adipose tissue, which contributes to worsened metabolic disorders, including more severe fatty liver, increased local inflammation in adipose tissue, and impaired systemic glucose tolerance in KO mice on a high-fat diet.

conclusionsThis study demonstrates Ces1d is a crucial factor in maintaining lipid homeostasis in macrophages. Loss of Ces1d leads to metabolic dysregulation in macrophages and other immune cells during obesity.

Indexed as

LipaseLipid MetabolismMacrophagesAdipose TissueAnimalsDiet, High-FatHumansInflammationMaleMiceMice, Inbred C57BLMice, KnockoutObesitySignal TransductionTriglyceridesLipaseTriglyceridesCes1dImmunometabolismInflammationLipid signalingMacrophages

Identifiers

PMID40349771
PMCPMC12145999

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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.