Evidence map›Paper›PMID 41931905›Full record

ArticleRedox biology2026

Alpha-ketoglutarate accelerates granulocyte-monocyte progenitor differentiation and atherosclerotic plaque inflammation via oxoglutarate receptor 1.

Jiwei Zhao, Li Su, Wenhao Li, Sin Man Lam, Cen Yan, Taotao Zhou, Yalan Deng, Yuan Dong, Yuan Zhou, Guanghou Shui and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Redox 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

11 authors.

Jiwei ZhaoBeijing Institute of Hepatology, Beijing Youan Hospital, Capital Medical University, Beijing, 100069, China; Department of Science and Development, Beijing Youan Hospital, Capital Medical University, Beijing, 100069, China.
Li SuNeuroscience Research Institute, Peking University Center of Medical and Health Analysis, Peking University, Beijing, 100191, China.
Wenhao LiDepartment of Biomedical Informatics, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.
Sin Man LamLipidALL Technologies Company Limited, Changzhou, Jiangsu Province, 213022, China.
Cen YanBeijing Institute of Hepatology, Beijing Youan Hospital, Capital Medical University, Beijing, 100069, China; Department of Science and Development, Beijing Youan Hospital, Capital Medical University, Beijing, 100069, China.
Taotao ZhouBeijing Institute of Hepatology, Beijing Youan Hospital, Capital Medical University, Beijing, 100069, China; Department of Science and Development, Beijing Youan Hospital, Capital Medical University, Beijing, 100069, China.
Yalan DengBeijing Institute of Hepatology, Beijing Youan Hospital, Capital Medical University, Beijing, 100069, China; Department of Science and Development, Beijing Youan Hospital, Capital Medical University, Beijing, 100069, China.
Yuan DongBeijing Institute of Hepatology, Beijing Youan Hospital, Capital Medical University, Beijing, 100069, China; Department of Science and Development, Beijing Youan Hospital, Capital Medical University, Beijing, 100069, China; Laboratory of Clinical Medicine, Capital Medical University, Beijing, 100069, China.
Yuan ZhouDepartment of Biomedical Informatics, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University, Beijing, 100191, China. Electronic address: zhouyuanbioinfo@bjmu.edu.cn.
Guanghou ShuiGuangzhou Laboratory, Guangzhou, Guangdong, 510005, China. Electronic address: shui_guanghou@gzlab.ac.cn.
Yingmei FengBeijing Institute of Hepatology, Beijing Youan Hospital, Capital Medical University, Beijing, 100069, China; Department of Science and Development, Beijing Youan Hospital, Capital Medical University, Beijing, 100069, China. Electronic address: yingmeif13@ccmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidence shows that excess cholesterol and glucose uptake stimulates the expansion of hematopoietic stem/progenitor cells and myeloid progenitors, resulting in increased production of inflammatory cells and atherosclerotic progression. However, the role of other metabolites in plaque progression remains unclear. Hereby, we observed elevated α-ketoglutarate levels in granulocyte-monocyte progenitors (GMPs) of Ldlr

Indexed as

Cell DifferentiationGranulocytesInflammationKetoglutaric AcidsPlaque, AtheroscleroticAnimalsAtherosclerosisDiet, High-FatHumansMiceMice, KnockoutMonocytesReceptors, LDLKetoglutaric AcidsReceptors, LDLAtherosclerosisGranulocyte-monocyte progenitorMyeloid cellPurine nucleoside phosphorylaseα-ketoglutarate

Identifiers

PMID41931905
PMCPMC13085009

What OpenQuestion holds

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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.