Evidence map›Paper›PMID 34592792›Full record

ArticleAging cell2021

miR-195-3p alleviates homocysteine-mediated atherosclerosis by targeting IL-31 through its epigenetics modifications.

Jiantuan Xiong, Fang Ma, Ning Ding, Lingbo Xu, Shengchao Ma, Anning Yang, Yinju Hao, Huiping Zhang, Yideng Jiang

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing 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

25 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Review
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  9. Article
  10. Linking homocysteine and ferroptosis in cardiovascular disease: insights and implications.Apoptosis : an international journal on programmed cell death · 2024
    Review
  11. Article
  12. Review
  13. Article
  14. Ferroptosis in Osteocytes as a Target for Protection Against Postmenopausal Osteoporosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  15. Article
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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

9 authors at 1 institution in 1 country.

Jiantuan XiongSchool of Basic Medical Sciences, Ningxia Medical University, Yinchuan, China.
Fang MaSchool of Basic Medical Sciences, Ningxia Medical University, Yinchuan, China.
Ning DingSchool of Basic Medical Sciences, Ningxia Medical University, Yinchuan, China.
Lingbo XuSchool of Basic Medical Sciences, Ningxia Medical University, Yinchuan, China.
Shengchao MaSchool of Basic Medical Sciences, Ningxia Medical University, Yinchuan, China.
Anning YangSchool of Basic Medical Sciences, Ningxia Medical University, Yinchuan, China.
Yinju HaoSchool of Basic Medical Sciences, Ningxia Medical University, Yinchuan, China.
Huiping ZhangNHC Key Laboratory of Metabolic Cardiovascular Diseases Research, Ningxia Medical University, Yinchuan, China.
Yideng JiangSchool of Basic Medical Sciences, Ningxia Medical University, Yinchuan, China.ORCID 0000-0002-4882-5197
Ningxia Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis is a serious age-related disease, which has a tremendous impact on health care globally. Macrophage inflammation is crucial for the initiation and progression of atherosclerosis, and microRNAs (miRNAs) recently have emerged as potent modulators of inflammation, while the underlying mechanisms of its involvement in homocysteine (Hcy)-mediated macrophage inflammation of atherosclerosis remain largely unknown. Here, we demonstrated that elevated Hcy inhibits the expression of miR-195-3p, which in turn enhances IL-31 expression and thereby causes the secretion of macrophages pro-inflammatory factors IL-1β, IL-6 and TNF-α and accelerate atherosclerosis. Furthermore, we identified that Hcy can induce DNA hypermethylation and H3K9 deacetylation of miR-195-3p promoter due to the increased the binding of DNMT3a and HDAC11 at its promoter. More importantly, Sp1 interacts with DNMT3a suppressed the binding of HDAC11 at miR-195-3p promoter and promoted its transcription. In summary, our results revealed a novel mechanism that transcriptional and epigenetic regulation of miR-195-3p inhibits macrophage inflammation through targeting IL-31, which provides a candidate diagnostic marker and novel therapeutic target in cardiovascular diseases induced by Hcy.

Indexed as

AnimalsApoptosisAtherosclerosisDNA MethylationEpigenesis, GeneticHomocysteineHumansInterleukinsMiceHomocysteineIL31 protein, humanInterleukinsDNA methylationH3K9 acetylationhomocysteineinflammationmiR-195-3p

Identifiers

PMID34592792
PMCPMC8520716
OpenAlexW3202664603

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.