Evidence map›Paper›PMID 40448300›Full record

ArticleInternational journal of experimental pathology2025

The role of ketone bodies in oxidized LDL-induced cell proliferation and lipid accumulation of macrophages.

Akira Sato, Hina Nemoto, Ayano Yabuki, Genta Sato, Yuta Ogawa, Makoto Ohira

Abstract read
In one paragraph

Article in International journal of experimental pathology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

6 authors.

Akira SatoDepartment of Food and Nutritional Science, Faculty of Human Life Science, Miyagi Gakuin Women's University, Sendai, Miyagi, Japan.ORCID 0000-0001-7015-4038
Hina NemotoFaculty of Pharmacy, Iryo Sosei University, Iwaki, Fukushima, Japan.
Ayano YabukiFaculty of Pharmacy, Iryo Sosei University, Iwaki, Fukushima, Japan.
Genta SatoFaculty of Pharmacy, Iryo Sosei University, Iwaki, Fukushima, Japan.
Yuta OgawaFaculty of Pharmacy, Iryo Sosei University, Iwaki, Fukushima, Japan.
Makoto OhiraFaculty of Pharmacy, Iryo Sosei University, Iwaki, Fukushima, Japan.ORCID 0000-0002-6629-8837

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ketone bodies (KBs), which include β-hydroxybutyric acid (β-HB) and acetoacetic acid (AcAc), play critical roles in organismal energy homeostasis; however, their effects on atherosclerosis remain unknown. In this study, we investigated the role of β-HB and AcAc on proliferation and lipid accumulation in macrophages by the uptake of oxidized LDL (Ox-LDL), causing the formation of atherosclerotic plaques, using mouse macrophage J774A.1 cells. Both β-HB and AcAc reduced cell proliferation, and AcAc increased lipid accumulation in Ox-LDL-treated J774A.1 cells. Western blotting showed that Ox-LDL decreased the protein expression of two KB-specific receptors, GPR41 and GPR43, both of which are known as potent modulators of inflammation, but had negligible effects on that of the β-HB-specific GPR109A in the cells. These results suggest that Ox-LDL may induce inflammatory responses by decreasing the protein expression of GPR41 and GPR43 in macrophages, and that AcAc, but not β-HB, may exacerbate Ox-LDL-caused atherosclerosis.

Indexed as

AtherosclerosisCell ProliferationKetone BodiesLipid MetabolismLipoproteins, LDLMacrophages3-Hydroxybutyric AcidAnimalsCell LineMicePlaque, AtheroscleroticReceptors, G-Protein-Coupled3-Hydroxybutyric AcidKetone BodiesLipoproteins, LDLoxidized low density lipoproteinReceptors, G-Protein-CoupledacetoacetateG‐protein coupled receptorketone bodieslipid accumulationmacrophageoxidized LDLproliferationβ‐hydroxybutyric acid

Identifiers

PMID40448300
PMCPMC12124991

What OpenQuestion holds

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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.