Evidence map›Paper›PMID 37142272›Full record

ArticleAging2023

Exosomal miR-663b from "M1" macrophages promotes pulmonary artery vascular smooth muscle cell dysfunction through inhibiting the AMPK/Sirt1 axis.

Honghong Ma, Yang Yu, Lirong Mo, Qian Chen, Hui Dong, Yan Xu, Bing Zhuan

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2023. 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
2.8field-weighted citation impact, top 10% 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, 18 citations in OpenAlex.

  1. Review
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  9. Signaling pathways and targeted therapy for pulmonary hypertension.Signal transduction and targeted therapy · 2025
    Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. The role and mechanism of AMPK in pulmonary hypertension.Therapeutic advances in respiratory disease
    Review
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

7 authors at 3 institutions in 1 country.

Honghong MaDepartment of Respiratory Medicine, People’s Hospital of Ningxia Hui Autonomous Region, Yinchuan 750000, Ningxia, China.
Yang YuCollege of Traditional Chinese Medicine, Ningxia Medical University, Yinchuan 750000, Ningxia, China.
Lirong MoDepartment of Respiratory Medicine, People’s Hospital of Ningxia Hui Autonomous Region, Yinchuan 750000, Ningxia, China.
Qian ChenDepartment of Respiratory Medicine, People’s Hospital of Ningxia Hui Autonomous Region, Yinchuan 750000, Ningxia, China.
Hui DongGeneral Hospital of Ningxia Medical University, Yinchuan 750000, Ningxia, China.
Yan XuCollege of Traditional Chinese Medicine, Ningxia Medical University, Yinchuan 750000, Ningxia, China.
Bing ZhuanDepartment of Respiratory Medicine, People’s Hospital of Ningxia Hui Autonomous Region, Yinchuan 750000, Ningxia, China.
Ningxia Medical University · CNNingxia Hui Autonomous Region Peoples Hospital · CNThe Fourth People's Hospital of Ningxia Hui Autonomous Region · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInflammatory mediators from macrophages are proven to be involved in pulmonary vascular remodeling in pulmonary hypertension (PH). Here, this study intends to explore the mechanism of "M1" macrophage-derived exosomal miR-663b in pulmonary artery smooth muscle cells (PASMCs) dysfunctions and pulmonary hypertension.

methodsHypoxia-treated PASMCs were utilized for constructing an

resultsmiR-663b was obviously up-regulated in hypoxia-elicited PASMCs and M1 macrophages. miR-663b overexpression boosted hypoxia-induced proliferation, inflammation, oxidative stress, and migration in PASMCs, whereas miR-663b low expression resulted in the opposite situation. AMPK was identified as a target of miR-663b, and miR-663b overexpression curbed the AMPK/Sirt1 pathway. AMPK activation ameliorated the damaging impact of miR-663b overexpression and "M1" macrophage exosomes on PASMCs.

conclusionExosomal miR-663b from "M1" macrophage facilitates PASMC dysfunctions and PH development by dampening the AMPK/Sirt1 axis.

Indexed as

Hypertension, PulmonaryMicroRNAsAMP-Activated Protein KinasesAnimalsCell ProliferationCells, CulturedHypoxiaMacrophagesMuscle, Smooth, VascularMyocytes, Smooth MusclePulmonary ArteryRatsSirtuin 1Vascular RemodelingAMP-Activated Protein KinasesMicroRNAsSirt1 protein, ratSirtuin 1AMPK pathwayexosomesmacrophagesmiR-663bpulmonary artery vascular smooth muscle cells

Identifiers

PMID37142272
PMCPMC10449306
OpenAlexW4372335458

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.