Evidence map›Paper›PMID 32843584›Full record

ArticleAging2020

Circulating exosomal miR-144-3p inhibits the mobilization of endothelial progenitor cells post myocardial infarction via regulating the MMP9 pathway.

Yihai Liu, Jiamin Xu, Rong Gu, Zhu Li, Kun Wang, Yu Qi, Xuan Sun, Jun Xie, Lian Wang, Biao Xu and 1 more

Open access · greenAbstract read
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. miR-144/451: A Regulatory Role in Inflammation.Current molecular medicine · 2025
    Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Exosomal microRNAs in diabetic heart disease.Cardiovascular diabetology · 2022
    Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. 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

11 authors at 1 institution in 1 country.

Yihai LiuDepartment of Cardiology, Nanjing Drum Tower Hospital, Clinical College of Nanjing Medical University, Nanjing 210008, China.
Jiamin XuDepartment of Cardiology, Nanjing Drum Tower Hospital, Nanjing University Medical School, Nanjing 210008, Jiangsu, China.
Rong GuDepartment of Cardiology, Nanjing Drum Tower Hospital, Nanjing University Medical School, Nanjing 210008, Jiangsu, China.
Zhu LiDepartment of Cardiology, Nanjing Drum Tower Hospital, Nanjing University Medical School, Nanjing 210008, Jiangsu, China.
Kun WangDepartment of Cardiology, Nanjing Drum Tower Hospital, Nanjing University Medical School, Nanjing 210008, Jiangsu, China.
Yu QiDepartment of Cardiology, Nanjing Drum Tower Hospital, Nanjing University Medical School, Nanjing 210008, Jiangsu, China.
Xuan SunDepartment of Cardiology, Nanjing Drum Tower Hospital, Nanjing University Medical School, Nanjing 210008, Jiangsu, China.
Jun XieDepartment of Cardiology, Nanjing Drum Tower Hospital, Nanjing University Medical School, Nanjing 210008, Jiangsu, China.
Lian WangDepartment of Cardiology, Nanjing Drum Tower Hospital, Nanjing University Medical School, Nanjing 210008, Jiangsu, China.
Biao XuDepartment of Cardiology, Nanjing Drum Tower Hospital, Clinical College of Nanjing Medical University, Nanjing 210008, China.
Lina KangDepartment of Cardiology, Nanjing Drum Tower Hospital, Clinical College of Nanjing Medical University, Nanjing 210008, China.
Nanjing Drum Tower Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe angiogenesis post myocardial infarction (MI) is compromised in diabetes. MiR-144-3p is reported to be highly expressed in circulating exosomes of diabetic patients, implying its role in diabetic complications. However, whether circulating exosomes and enriched miR-144-3p are involved in the impaired neovascularization in diabetes and the underlying mechanism is unclear.

resultsDMexo and miR-144-3p mimic-treated MSCs had elevated miR-144-3p levels and decreased MMP9, Ets1 and PLG expression. The percentage of EPCs were relatively lower in DMexo-treated or agomir-treated MI mice compared with MI mice. Finally, the luciferase assay confirmed the direct binding between miR-144-3p and Ets1.

conclusionExosomal miR-144-3p could impair the mobilization ability of EPCs, which was associated with impaired ischemia-induced neovascularization.

methodsCirculating exosomes were isolated from Streptozotocin (STZ)-induced mice.

Indexed as

Cell MovementNeovascularization, Physiologic3' Untranslated RegionsAnimalsBinding SitesCells, CulturedCirculating MicroRNADiabetes Mellitus, ExperimentalEndothelial Progenitor CellsExosomesMaleMatrix Metalloproteinase 9Mice, Inbred C57BLMicroRNAsMyocardial InfarctionProto-Oncogene Protein c-ets-13' Untranslated RegionsCirculating MicroRNAEts1 protein, mouseMatrix Metalloproteinase 9MicroRNAsMIRN144 microRNA, mouseMmp9 protein, mouseProto-Oncogene Protein c-ets-1diabetesendothelial progenitor cellsmiR-144-3pmyocardial infarction

Identifiers

PMID32843584
PMCPMC7485705
OpenAlexW3080432113

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.