Evidence map›Paper›PMID 38045055›Full record

ArticleActa pharmaceutica Sinica. B2023

ADAR1 regulates vascular remodeling in hypoxic pulmonary hypertension through

Junting Zhang, Yiying Li, Jianchao Zhang, Lu Liu, Yuan Chen, Xusheng Yang, Xueyi Liao, Muhua He, Zihui Jia, Jun Fan and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta pharmaceutica Sinica. B, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
–field-weighted citation impact
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

21 citing papers in PubMed.

  1. Article
  2. Review
  3. HBiomedicines · 2026
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Targeting RNA adenosine editing and modification enzymes for RNA therapeutics.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Review
  14. Review
  15. Review
  16. The role of ADAR1 in human pathophysiology.Frontiers in cell and developmental biology · 2025
    Review
  17. Review
  18. Article
  19. Review
  20. 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

12 authors.

Junting ZhangShenzhen Institute of Respiratory Disease, Shenzhen Key Laboratory of Respiratory Disease, Shenzhen People's Hospital (the Second Clinical Medical College, Jinan University; the First Affiliated Hospital, Southern University of Science and Technology), Shenzhen 518020, China; Post-Doctoral Scientific Research Station of Basic Medicine, Jinan University, Guangzhou 510632, China.
Yiying LiShenzhen Institute of Respiratory Disease, Shenzhen Key Laboratory of Respiratory Disease, Shenzhen People's Hospital (the Second Clinical Medical College, Jinan University; the First Affiliated Hospital, Southern University of Science and Technology), Shenzhen 518020, China; Post-Doctoral Scientific Research Station of Basic Medicine, Jinan University, Guangzhou 510632, China.
Jianchao ZhangShenzhen Institute of Respiratory Disease, Shenzhen Key Laboratory of Respiratory Disease, Shenzhen People's Hospital (the Second Clinical Medical College, Jinan University; the First Affiliated Hospital, Southern University of Science and Technology), Shenzhen 518020, China; Post-Doctoral Scientific Research Station of Basic Medicine, Jinan University, Guangzhou 510632, China.
Lu LiuDepartment of Pharmacology, School of Medicine, Southern University of Science and Technology, Shenzhen 518055, China.
Yuan ChenLung Transplant Group, Wuxi People's Hospital Affiliated to Nanjing Medical University, Wuxi 211103, China.
Xusheng YangLung Transplant Group, Wuxi People's Hospital Affiliated to Nanjing Medical University, Wuxi 211103, China.
Xueyi LiaoShenzhen Institute of Respiratory Disease, Shenzhen Key Laboratory of Respiratory Disease, Shenzhen People's Hospital (the Second Clinical Medical College, Jinan University; the First Affiliated Hospital, Southern University of Science and Technology), Shenzhen 518020, China; Post-Doctoral Scientific Research Station of Basic Medicine, Jinan University, Guangzhou 510632, China.
Muhua HeDepartment of Pharmacology, School of Medicine, Southern University of Science and Technology, Shenzhen 518055, China.
Zihui JiaLung Transplant Group, Wuxi People's Hospital Affiliated to Nanjing Medical University, Wuxi 211103, China.
Jun FanDepartment of Medical Biochemistry and Molecular Biology, School of Medicine, Jinan University, Guangzhou 510632, China.
Jin-Song BianDepartment of Pharmacology, School of Medicine, Southern University of Science and Technology, Shenzhen 518055, China.
Xiaowei NieShenzhen Institute of Respiratory Disease, Shenzhen Key Laboratory of Respiratory Disease, Shenzhen People's Hospital (the Second Clinical Medical College, Jinan University; the First Affiliated Hospital, Southern University of Science and Technology), Shenzhen 518020, China; Post-Doctoral Scientific Research Station of Basic Medicine, Jinan University, Guangzhou 510632, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary hypertension (PH) is an extremely malignant pulmonary vascular disease of unknown etiology. ADAR1 is an RNA editing enzyme that converts adenosine in RNA to inosine, thereby affecting RNA expression. However, the role of ADAR1 in PH development remains unclear. In the present study, we investigated the biological role and molecular mechanism of ADAR1 in PH pulmonary vascular remodeling. Overexpression of ADAR1 aggravated PH progression and promoted the proliferation of pulmonary artery smooth muscle cells (PASMCs). Conversely, inhibition of ADAR1 produced opposite effects. High-throughput whole transcriptome sequencing showed that ADAR1 was an important regulator of circRNAs in PH. CircCDK17 level was significantly lowered in the serum of PH patients. The effects of ADAR1 on cell cycle progression and proliferation were mediated by circCDK17. ADAR1 affects the stability of circCDK17 by mediating A-to-I modification at the A5 and A293 sites of circCDK17 to prevent it from m1A modification. We demonstrate for the first time that ADAR1 contributes to the PH development, at least partially, through m1A modification of circCDK17 and the subsequent PASMCs proliferation. Our study provides a novel therapeutic strategy for treatment of PH and the evidence for circCDK17 as a potential novel marker for the diagnosis of this disease.

Indexed as

ADAR1Cell proliferationCircular RNAPulmonary hypertensionVascular remodeling

Identifiers

PMID38045055
PMCPMC10692360

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.