Evidence map›Paper›PMID 33687636›Full record

ArticleBiochemical genetics2021

LncRNA HOXA-AS3 Promotes the Progression of Pulmonary Arterial Hypertension through Mediation of miR-675-3p/PDE5A Axis.

Zhong-Kui Li, Lu-Fang Gao, Xi-An Zhu, Dao-Kang Xiang

Abstract read
PubMed Publisher
In one paragraph

Article in Biochemical genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Roles of LncRNAs in the Pathogenesis of Pulmonary Hypertension.Reviews in cardiovascular medicine · 2024
    Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. The integrated comprehension of lncRNA HOXA-AS3 implication on human diseases.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Review
  11. Review
  12. 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

4 authors at 1 institution in 1 country.

Zhong-Kui LiDepartment of Cardiovascular Surgery, Guizhou Provincial People's Hospital, No.83, East Zhongshan Road, Guiyang, 550002, Guizhou Province, People's Republic of China.
Lu-Fang GaoDepartment of Cardiovascular Surgery, Guizhou Provincial People's Hospital, No.83, East Zhongshan Road, Guiyang, 550002, Guizhou Province, People's Republic of China.
Xi-An ZhuDepartment of Cardiovascular Surgery, Guizhou Provincial People's Hospital, No.83, East Zhongshan Road, Guiyang, 550002, Guizhou Province, People's Republic of China.
Dao-Kang XiangDepartment of Cardiovascular Surgery, Guizhou Provincial People's Hospital, No.83, East Zhongshan Road, Guiyang, 550002, Guizhou Province, People's Republic of China. xiangdk135@163.com.ORCID http://orcid.org/0000-0001-5272-3866
Guizhou Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) seriously threatens the elder people. Long non-coding RNAs (lncRNAs) are involved in multiple diseases. However, the study of the lncRNAs in the occurrence of PAH is just beginning. For this, we sought to explore the biological function of lncRNA HOXA cluster antisense RNA 3 (HOXA-AS3) in PAH. Hypoxia (HYP) was used to mimic in vitro model of PAH. Gene and protein expressions in cells were detected by q-PCR and Western blotting, respectively. In addition, cell proliferation and viability were tested by CCK-8 and MTT assay. Cell apoptosis was measured by flow cytometry. Wound healing was used to detect cell migration. Furthermore, the connection of HOXA-AS3, miR-675-3p, and phosphodiesterase 5A (PDE5A) was verified by dual-luciferase report assay. HOXA-AS3 and PDE5A were upregulated in human pulmonary artery smooth muscle cells (HPASMCs) in the presence of HYP, while miR-675-3p was downregulated. Moreover, knockdown of HOXA-AS3 suppressed the growth and migration of HPASMCs, but induced the apoptosis. Overexpression of miR-675-3p achieved the same effect. MiR-675-3p inhibitor or overexpression of PDE5A notably reversed the inhibitory effect of HOXA-AS3 knockdown on PAH. Finally, HOXA-AS3 could sponge miR-675-3p, and PDE5A was directly targeted by miR-675-3p. HOXA-AS3 increased the development of PAH via regulation of miR-675-3p/PDE5 axis, which could be the potential biomarker for treatment of PAH.

Indexed as

Gene Expression Regulation, NeoplasticApoptosisBiomarkersCell MovementCell ProliferationCells, CulturedCyclic Nucleotide Phosphodiesterases, Type 5Homeodomain ProteinsHumansMicroRNAsPulmonary Arterial HypertensionRNA, AntisenseRNA, Long NoncodingBiomarkersCyclic Nucleotide Phosphodiesterases, Type 5Homeodomain ProteinsHoxA proteinMicroRNAsMIRN675 microRNA, humanPDE5A protein, humanRNA, AntisenseRNA, Long NoncodingHOXA cluster antisense RNA 3MiR-675-3pPhosphodiesterase 5APulmonary arterial hypertension

Identifiers

PMID33687636
OpenAlexW3135069506

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.