Evidence map›Paper›PMID 39698913›Full record

ArticleJournal of cellular and molecular medicine2024

Indole-3-Carboxaldehyde Inhibits Inflammatory Response and Lipid Accumulation in Macrophages Through the miR-1271-5p/HDAC9 Pathway.

Wei Luo, Jun Meng, Xiao-Hua Yu, Zi-Zhen Zhang, Gang Wang, Jin He

Abstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Indole-3-Carbaldehyde fromResearch (Washington, D.C.) · 2026
    Article
  8. Review
  9. Research Status and Latest Progress in the Regulatory Mechanisms of ABCA1.International journal of molecular sciences · 2025
    Review
  10. Article
  11. Article
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.

Wei LuoThe First Affiliated Hospital, Department of Cardiology, Hengyang Medical School, University of South China, Hengyang, Hunan, China.ORCID 0009-0003-2880-4887
Jun MengThe First Affiliated Hospital, Department of Function, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Xiao-Hua YuInstitute of Clinical Medicine, The Second Affiliated Hospital of Hainan Medical University, Haikou, Hainan, China.
Zi-Zhen ZhangSchool of Medical and Pharmacological Technology, Hunan Polytechnic of Environment and Biology, Hengyang, Hunan, China.
Gang WangThe First Affiliated Hospital, Department of Cardiology, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Jin HeThe First Affiliated Hospital, Department of Function, Hengyang Medical School, University of South China, Hengyang, Hunan, China.

Funding

National Natural Science Foundation of China 82060086Natural Science Foundation of Hunan Province 2022JJ30533Natural Science Foundation of Hunan Province 2022JJ60050Natural Science Foundation of Hunan Province 2024JJ9364Scientific Research Project of Hunan Provincial Health Commission 202102061915Scientific Research Project of Hunan Provincial Health Commission B202303017063
6 · The paper itself

Abstract

Indole-3-carboxaldehyde (ICA), a microbiota-derived tryptophan metabolite, has been reported to protect against atherosclerosis. However, the molecular mechanisms for its atheroprotective effect remain largely unknown. This study aimed to explore the influence of ICA on lipid accumulation and inflammatory response in THP-1 macrophage-derived foam cells. Our results showed that administration of ICA upregulated the expression of miR-1271-5p, ATP binding cassette transporter A1 (ABCA1) and ABCG1, downregulated histone deacetylase 9 (HDAC9) expression and inhibited macrophage lipid accumulation. ICA treatment also facilitated macrophage polarisation to the M2 phenotype and alleviated inflammatory response, as evidenced by decreased IL-6 levels and increased IL-10 levels. HDAC9 was identified as a direct target of miR-1271-5p. HDAC9 overexpression or miR-1271-5p knockdown decreased the effect of ICA on ABCA1 and ABCG1 expression as well as inflammatory response. Taken together, these results suggest that ICA can suppress lipid accumulation and mitigate inflammatory response in macrophages by activating the miR-1271-5p/HDAC9 signalling cascade, thereby providing new explanations for how ICA reduces atherosclerosis.

Indexed as

ATP Binding Cassette Transporter 1ATP Binding Cassette Transporter, Subfamily G, Member 1Histone DeacetylasesIndolesInflammationLipid MetabolismMacrophagesMicroRNAsSignal TransductionAtherosclerosisFoam CellsGene Expression RegulationHumansRepressor ProteinsTHP-1 CellsABCA1 protein, humanABCG1 protein, humanATP Binding Cassette Transporter 1ATP Binding Cassette Transporter, Subfamily G, Member 1HDAC9 protein, humanHistone DeacetylasesIndolesMicroRNAsRepressor ProteinsatherosclerosisHDAC9ICAinflammatory responselipid accumulationmiR‐1271‐5p

Identifiers

PMID39698913
PMCPMC11656405

What Socratic 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 Socratic graph.