Evidence map›Paper›PMID 30639412›Full record

ArticleJournal of molecular and cellular cardiology2019

Macrophage fatty acid oxidation inhibits atherosclerosis progression.

Mitsunori Nomura, Jie Liu, Zu-Xi Yu, Tomoko Yamazaki, Ye Yan, Hiroyuki Kawagishi, Ilsa I Rovira, Chengyu Liu, Michael J Wolfgang, Yoh-Suke Mukouyama and 1 more

Open access · greenAbstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.0field-weighted citation impact, top 13% of its field
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

43 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
  2. Macrophage PIM1 Drives Atherosclerosis by Enhancing Foam Cell Formation Via CD36.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Lipid metabolism in homeostasis and disease.Signal transduction and targeted therapy · 2026
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Macrophage energy metabolism in cardiometabolic disease.Molecular and cellular biochemistry · 2025
    Review
  16. Review
  17. Mechanisms of metabolic reprogramming in abdominal aortic aneurysm.Frontiers in cell and developmental biology · 2025
    Review
  18. Review
  19. Progress in macrophage immune regulation of atherosclerosis.American journal of translational research · 2025
    Review
  20. Review
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

11 authors at 2 institutions in 1 country.

Mitsunori NomuraCenter for Molecular Medicine, NIH, National Heart, Lung, and Blood Institute, Bethesda, MD 20892, USA; Laboratory of Stem Cell and Neuro-Vascular Biology, Genetics and Developmental Biology Center, NIH, National Heart, Lung, and Blood Institute, Bethesda, MD 20892, USA.
Jie LiuCenter for Molecular Medicine, NIH, National Heart, Lung, and Blood Institute, Bethesda, MD 20892, USA; Aging Institute, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA.
Zu-Xi YuNIH, Pathology Core, National Heart, Lung, and Blood Institute, Bethesda, MD 20892, USA.
Tomoko YamazakiLaboratory of Stem Cell and Neuro-Vascular Biology, Genetics and Developmental Biology Center, NIH, National Heart, Lung, and Blood Institute, Bethesda, MD 20892, USA; Robert W. Franz Cancer Center, Providence Portland Medical Center, Earle A. Chiles Research Institute, Portland, OR 97213, USA.
Ye YanCenter for Molecular Medicine, NIH, National Heart, Lung, and Blood Institute, Bethesda, MD 20892, USA.
Hiroyuki KawagishiCenter for Molecular Medicine, NIH, National Heart, Lung, and Blood Institute, Bethesda, MD 20892, USA.
Ilsa I RoviraCenter for Molecular Medicine, NIH, National Heart, Lung, and Blood Institute, Bethesda, MD 20892, USA.
Chengyu LiuNIH, Transgenic Core, National Heart, Lung, and Blood Institute, Bethesda, MD 20892, USA.
Michael J WolfgangDepartment of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Yoh-Suke MukouyamaLaboratory of Stem Cell and Neuro-Vascular Biology, Genetics and Developmental Biology Center, NIH, National Heart, Lung, and Blood Institute, Bethesda, MD 20892, USA.
Toren FinkelCenter for Molecular Medicine, NIH, National Heart, Lung, and Blood Institute, Bethesda, MD 20892, USA; Aging Institute, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA. Electronic address: finkelt@pitt.edu.
National Heart Lung and Blood Institute · USJohns Hopkins University · US

Funding

Transgenic CoreZICHL005907 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI LIU, CHENGYU · 2010 to 2025
$25.8M
The study of stem cell and neuro-vascular developmentZIAHL005702 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI MUKOUYAMA, YOH-SUKE · 2009 to 2025
$14.9M
Pathology CoreZICHL005904 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI YU, ZU XI · 2010 to 2023
$11.6M
FACSZ01HL005905 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI FINKEL, TOREN · 2008 to 2008
$660k
Intramural NIH HHS Z01 HL005905Intramural NIH HHS ZIC HL005907
6 · The paper itself

Abstract

Atherosclerosis is a chronic disorder of the vessel wall. One key regulator of disease progression is lipid handling in macrophages. However, the role of macrophage mitochondrial-dependent fatty acid β-oxidation (FAO) in atherosclerosis is not well defined. To address this, we focused on carnitine palmitoyltransferase (CPT) 1 and 2, which play an essential role in the transport of long chain fatty acids (FAs) into the mitochondria. Using conditional alleles of these mitochondrial enzymes, we have generated myeloid-specific Cpt1a and Cpt2 knockout mutants (CPT1a M-KO and CPT2 M-KO). In culture, macrophages derived from CPT1a and CPT2 M-KO mice have impaired FAO, enhanced expression of the CD36 scavenger receptor, increased uptake of oxidized low-density lipoprotein (oxLDL), and augmented transformation into cholesterol-rich foam cells. In line with these in vitro observations, in the atherosclerosis-susceptible apolipoprotein E (ApoE) KO background, CPT2 M-KO mice demonstrated augmented atherosclerosis, accompanied by increased accumulation of aortic macrophages with elevated CD36 expression. These data suggest that macrophage FAO is athero-protective and that augmenting FAO may potentially slow atherosclerotic progression.

Indexed as

Disease ProgressionAnimalsAtherosclerosisFatty AcidsMacrophagesMiceMice, KnockoutMyeloid CellsOxidation-ReductionFatty Acids

Identifiers

PMID30639412
PMCPMC9124604
OpenAlexW2909548282

What OpenQuestion holds

Textmetadata
LicenceTDM
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.