Evidence map›Paper›PMID 37185889›Full record

ArticleCell death & disease2023

Butyrate dictates ferroptosis sensitivity through FFAR2-mTOR signaling.

GuoYan Wang, SenLin Qin, Lei Chen, HuiJun Geng, YiNing Zheng, Chao Xia, JunHu Yao, Lu Deng

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
16.3field-weighted citation impact, top 1% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

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  17. Gut Microbial Metabolism in Colorectal Cancer.Methods in molecular biology (Clifton, N.J.) · 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 2 institutions in 1 country.

GuoYan Wang *College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi, 712100, China.
SenLin Qin *College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi, 712100, China.
Lei Chen *Division of Laboratory Safety and Services, Northwest A&F University, Yangling, Shaanxi, 712100, China.
HuiJun GengCollege of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi, 712100, China.
YiNing ZhengCollege of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi, 712100, China.
Chao XiaCollege of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi, 712100, China.
JunHu YaoCollege of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi, 712100, China. yaojunhu2008@nwafu.edu.cn.
Lu DengCollege of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi, 712100, China. denglu128128@nwafu.edu.cn.ORCID 0000-0002-3744-4102
Northwest A&F University · CNNorth West Agriculture and Forestry University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Evidence shows that short-chain fatty acids (SCFAs) play an important role in health maintenance and disease development. In particular, butyrate is known to induce apoptosis and autophagy. However, it remains largely unclear whether butyrate can regulate cell ferroptosis, and the mechanism by which has not been studied. In this study, we found that RAS-selective lethal compound 3 (RSL3)- and erastin-induced cell ferroptosis were enhanced by sodium butyrate (NaB). With regard to the underlying mechanism, our results showed that NaB promoted ferroptosis by inducing lipid ROS production via downregulating the expression of solute carrier family 7 member 11 (SLC7A11) and glutathione peroxidase 4 (GPX4). Moreover, the FFAR2-AKT-NRF2 axis and FFAR2-mTORC1 axis accounts for the NaB-mediated downregulation of SLC7A11 and GPX4, respectively, in a cAMP-PKA-dependent manner. Functionally, we found that NaB can inhibit tumor growth and the inhibitory effect could be eliminated by administrating MHY1485 (mTORC1 activator) and Ferr-1 (ferroptosis inhibitor). Altogether, in vivo results suggest that NaB treatment is correlated to the mTOR-dependent ferroptosis and consequent tumor growth through xenografts and colitis-associated colorectal tumorigenesis, implicating the potential clinical applications of NaB for future colorectal cancer treatments. Based on all these findings, we have proposed a regulatory mechanism via which butyrate inhibits the mTOR pathway to control ferroptosis and consequent tumorigenesis.

Indexed as

FerroptosisButyric AcidCarcinogenesisCell Transformation, NeoplasticHumansMechanistic Target of Rapamycin Complex 1Receptors, G-Protein-CoupledTOR Serine-Threonine KinasesButyric AcidFFAR2 protein, humanMechanistic Target of Rapamycin Complex 1MTOR protein, humanReceptors, G-Protein-CoupledTOR Serine-Threonine Kinases

Identifiers

PMID37185889
PMCPMC10130170
OpenAlexW4366986939

What OpenQuestion holds

Textmetadata
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.