Evidence map›Paper›PMID 36557935›Full record

ArticleMolecules (Basel, Switzerland)2022

Short-Chain Fatty Acids Weaken Ox-LDL-Induced Cell Inflammatory Injury by Inhibiting the NLRP3/Caspase-1 Pathway and Affecting Cellular Metabolism in THP-1 Cells.

Chengxue Yi, Wen Sun, Longkun Ding, Man Yan, Chang Sun, Chenguang Qiu, Dongxu Wang, Liang Wu

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

20 citing papers in PubMed, 28 citations in OpenAlex.

  1. Journal of cell communication and signaling · 2026
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  3. [Gut-vascular axis in Kawasaki disease: short-chain fatty acid-mediated immune regulation and therapeutic targets].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026
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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

8 authors at 4 institutions in 1 country.

Chengxue YiSchool of Medical Technology, Zhenjiang College, Zhenjiang 212028, China.
Wen SunDepartment of Critical Care Medicine, Jurong People's Hospital, Jurong 212499, China.
Longkun DingDepartment of Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang 212013, China.
Man YanDepartment of Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang 212013, China.
Chang SunDepartment of Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang 212013, China.
Chenguang QiuStomatology Department, Zhenjiang First People's Hospital, Zhenjiang 212003, China.
Dongxu WangSchool of Grain Science and Technology, Jiangsu University of Science and Technology, Zhenjiang 212100, China.ORCID 0000-0001-7377-6190
Liang WuDepartment of Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang 212013, China.
Jiangsu University · CNCentral People's Hospital of Zhanjiang · CNJiangsu University of Science and Technology · CNYoujiang Medical College for Nationalities · CN

Funding

Science and Technology Planning Social Development Project of Zhenjiang City SH2020066, SH2021043, SH2021044, SH2021044 and FZ2020039
6 · The paper itself

Abstract

Short-chain fatty acids (SCFAs) are important anti-inflammatory metabolites of intestinal flora. Oxidized low-density lipoprotein (ox-LDL)-induced macrophage activation is critical for the formation of atherosclerosis plaque. However, the association between SCFAs and ox-LDL-induced macrophage activation with respect to the formation of atherosclerosis plaque has not yet been elucidated. The present study investigated whether SCFAs (sodium acetate, sodium propionate, and sodium butyrate) can affect ox-LDL-induced macrophage activation and potential signaling pathways via regulation of the expression of the NLRP3/Caspase-1 pathway. Using human monocyte-macrophage (THP-1) cells as a model system, it was observed that ox-LDL not only induced cell inflammatory injury but also activated the NLRP3/Caspase-1 pathway. The exogenous supplementation of three SCFAs could significantly inhibit cell inflammatory injury induced by ox-LDL. Moreover, three SCFAs decreased the expression of IL-1β and TNF-α via the inactivation of the NLRP3/Caspase-1 pathway induced by ox-LDL. Furthermore, three SCFAs affected cellular metabolism in ox-LDL-induced macrophages, as detected by untargeted metabolomics analysis. The results of the present study indicated that three SCFAs inhibited ox-LDL-induced cell inflammatory injury by blocking the NLRP3/Caspase-1 pathway, thereby improving cellular metabolism. These findings may provide novel insights into the role of SCFA intervention in the progression of atherosclerotic plaque formation.

Indexed as

AtherosclerosisNLR Family, Pyrin Domain-Containing 3 ProteinCaspase 1Fatty Acids, VolatileHumansLipoproteins, LDLTHP-1 CellsCaspase 1Fatty Acids, VolatileLipoproteins, LDLNLR Family, Pyrin Domain-Containing 3 Proteinoxidized low density lipoproteinanti-inflammationcellular metabolismmetabolomicsoxidized low-density lipoproteinshort chain fatty acids

Identifiers

PMID36557935
PMCPMC9786193
OpenAlexW4311154478

What OpenQuestion holds

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LicenceCC BY
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.