Evidence map›Paper›PMID 32588186›Full record

ArticleJournal of bioenergetics and biomembranes2020

Butyrate mitigates TNF-α-induced attachment of monocytes to endothelial cells.

Yan Wang, Yuanyuan Xu, Mao Yang, Mingyu Zhang, Mochao Xiao, Xueqi Li

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of bioenergetics and biomembranes, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.9field-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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
  2. [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

6 authors at 1 institution in 1 country.

Yan WangDepartment of Cardiology, the Fourth Hospital of Harbin Medical University, Harbin, 150001, Heilongjiang, China.
Yuanyuan XuDepartment of Cardiology, the Fourth Hospital of Harbin Medical University, Harbin, 150001, Heilongjiang, China.
Mao YangDepartment of Cardiology, the Fourth Hospital of Harbin Medical University, Harbin, 150001, Heilongjiang, China.
Mingyu ZhangDepartment of Cardiology, the Fourth Hospital of Harbin Medical University, Harbin, 150001, Heilongjiang, China.
Mochao XiaoDepartment of Cardiology, the Fourth Hospital of Harbin Medical University, Harbin, 150001, Heilongjiang, China.
Xueqi LiDepartment of Cardiology, the Fourth Hospital of Harbin Medical University, Harbin, 150001, Heilongjiang, China. xueqil67@163.com.ORCID 0000-0002-3509-302X
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A major cause of late-life health complications is the cardiovascular disease known as atherosclerosis. The process of atherogenesis is marked by endothelial cell dysfunction, the development of atherogenic lesions, and plaque buildup on the intima of the arterial endothelium. This process is fueled primarily by the adhesion of monocytes to endothelial cells via the actions of the cellular adhesion molecules VCAM-1 and E-selectin. When expressed at their basal levels, these molecules are vital to various cellular processes, but when in a state of overproduction, they drive the progression of atherosclerosis by recruiting monocytes to roll along and adhere to the endothelium. TNF-α is theorized to play a causal role in the development of atherosclerosis, but the exact mechanism remains poorly understood. This cytokine is known to upregulate various factors associated with inflammation and oxidative stress, both of which greatly contribute to endothelial dysfunction and atherogenesis. In the present study, we aimed to elucidate the effect of butyrate on these atherogenic processes. Previously not known to have atheroprotective effects, this natural compound shows promise as a treatment for atherosclerosis. In the present study, we found butyrate to exert various anti-inflammatory and downstream regulatory effects. Namely, butyrate ameliorated the overproduction of adhesion molecules, including VCAM-1 and E-selectin, reduced oxidative stress by reducing the levels of ROS and 4-HNE, and suppressed inflammation via inhibition of MCP-1 and IL-8. Additionally, butyrate rescued the reduced expression of the protective factor KLF2, which was mediated through the ERK5 pathway. Thus, butyrate may serve as a promising treatment against atherosclerosis.

Indexed as

ButyratesEndothelial CellsHumansMonocytesTumor Necrosis Factor-alphaButyratesTumor Necrosis Factor-alphaAdhesion moleculesAtherosclerosisButyrateE-selectinTNF-αVCAM-1

Identifiers

PMID32588186
OpenAlexW3037338938

What OpenQuestion holds

Textmetadata
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.