Evidence map›Paper›PMID 31949646›Full record

ArticleInternational journal of clinical and experimental pathology2018

TGF-β1/Smad3 signaling promotes collagen synthesis in pulmonary artery smooth muscle by down-regulating miR-29b.

Tingxia Wang, Yun Li, Juan Chen, Lijian Xie, Tingting Xiao

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.7field-weighted citation impact, top 25% 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

14 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Serum miR‑29 is increased in mice with early liver fibrosis.Experimental and therapeutic medicine · 2024
    Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Renoprotective Effect of Formononetin by Suppressing Smad3 Expression in Db/Db Mice.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020
    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

5 authors at 2 institutions in 1 country.

Tingxia WangDepartment of Cardiology, Shanghai Children's Hospital, Shanghai Jiao Tong University Shanghai, China.
Yun LiDepartment of Cardiology, Shanghai Children's Hospital, Shanghai Jiao Tong University Shanghai, China.
Juan ChenDepartment of Cardiology, Shanghai Children's Hospital, Shanghai Jiao Tong University Shanghai, China.
Lijian XieDepartment of Cardiology, Shanghai Children's Hospital, Shanghai Jiao Tong University Shanghai, China.
Tingting XiaoDepartment of Cardiology, Shanghai Children's Hospital, Shanghai Jiao Tong University Shanghai, China.
Shanghai Children's Hospital · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Deposition of fibronectin and collagen in the extracellular matrix (ECM) and the proliferation, migration, and hypertrophy of vascular smooth muscle cells (VSMCs) result in pulmonary arterial (PA) hypertrophy and muscularization, leading to increased pulmonary vascular resistance in pulmonary arterial hypertension (PAH). MicroRNA29 (miR-29) is reported to be associated with diseases such as liver fibrosis, renal fibrosis, pulmonary fibrosis, and cardiac fibrosis in which collagen synthesis plays an important role. Due to the possible link between PAH and collagen, in this study, we examined the role and therapeutic potential of miR-29b in vitro and in a rat model of pulmonary hypertension induced by monocrotaline (MCT). Results revealed that miR-29b treatment PAH rats showed a lower level of collagen synthesis. Furthermore, in pulmonary arterial smooth muscle cells (PASMCs), TGFβ1/Smad3 signaling negatively regulated the expression of miR-29b, and miR-29b suppressed collagen synthesis by directly targeting collagen I and blocking PI3K/AKT signaling. In addition, TGF-β1/Smad3 signaling promoted collagen synthesis in PASMCs by down-regulating miR-29b. Interestingly, Smad3 decreased the expression of miR-29b by interacting with its promotor. In conclusion, our results revealed that miR-29b plays an important role in collagen synthesis and may be a therapeutic target for PAH when regulated by the TGF-β1/Smad3 pathway.

Indexed as

collagen synthesismiR-29bPASMCsSmad3TGF-β1

Identifiers

PMID31949646
PMCPMC6963096
OpenAlexW3005080675

What OpenQuestion holds

Textmetadata
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.