Evidence map›Paper›PMID 40395196›Full record

ArticleArthritis & rheumatology (Hoboken, N.J.)2025

Activin A-Activated ALK4 Induces Pathogenic Th17-Involved Endothelial-Mesenchymal Transition in Systemic Lupus Erythematosus-Associated Pulmonary Arterial Hypertension.

Shuliang Jing, Junyan Qian, Hongjie Ying, Pei Mao, Mingxin Yao, Zhihong Wu, Harm J Bogaard, Lie Wang, Mengtao Li, Jun Yang

Abstract read
In one paragraph

Article in Arthritis & rheumatology (Hoboken, N.J.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Journal of thoracic disease · 2026
    Article
  3. Article
  4. Review
  5. Integrated single-cell TCR analysis across tissue identifies GZMKInternational journal of biological sciences · 2026
    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

10 authors.

Shuliang JingDepartment of Physiology and Department of Cardiology, the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Junyan QianDepartment of Rheumatology, Peking Union Medical College Hospital, Beijing, China.ORCID https://orcid.org/0000-0002-6909-539X
Hongjie YingDepartment of Physiology and Department of Cardiology, the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Pei MaoDepartment of Physiology and Department of Cardiology, the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Mingxin YaoDepartment of Physiology and Department of Cardiology, the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Zhihong WuStem Cell Facility of National Infrastructures for Translational Medicine, Institute of Clinical Medicine, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union College, Beijing, China.
Harm J BogaardDepartment of Pulmonary Medicine, Amsterdam University Medical Center Vrije University, Amsterdam, The Netherlands.
Lie WangDepartment of Immunology, School of Basic Medical Sciences, Zhejiang University School of Medicine, Hangzhou, China.
Mengtao LiDepartment of Rheumatology, Peking Union Medical College Hospital, Beijing, China.ORCID https://orcid.org/0000-0003-4252-2889
Jun YangDepartment of Physiology, and Department of Cardiology of the Second Affiliated Hospital, Zhejiang University School of Medicine and State Key Laboratory of Transvascular Implantation Devices, Hangzhou, China.ORCID https://orcid.org/0000-0001-9715-8100

Funding

Beijing Nova Program UHB11839National Key Research and Development Program of China 2021YFA1100500National Key Research and Development Program of China 2023YFC2507100the National Fundation Science of China 82470431
6 · The paper itself

Abstract

objectiveAutoimmune diseases, such as systemic lupus erythematosus (SLE), are associated with pulmonary arterial hypertension (PAH), a condition that can lead to heart failure. However, whether T cells also contribute to the occurrence of PAH in SLE has not been clarified. The objective of this study was to elucidate the role of Activin A and activated receptor signaling in SLE-PAH.

methodsMass Cytometry (CyTOF) analysis was performed to identify the major affected immune cell population in patients with SLE-PAH. Serum Activin A and interleukin-17 (IL-17) levels in patients with SLE-PAH, patients with SLE, and healthy donors were determined by enzyme-linked immunosorbent assay. Cocultures of Th17 cells with pulmonary microvascular endothelial cells (PMECs) and relevant rodent models were used to identify the converged target.

resultsThe reduced CD4

conclusionOur findings suggest that Activin A activates ALK4 in Th17 cells, thereby inducing IL-17 secretion. Concurrently, activated ALK4 induces EndoMT in human PMECs (hPMECs) via CTGF up-regulation. It suggests that ALK4 is a promising therapeutic target for SLE-PAH.

Indexed as

Activin Receptors, Type IActivinsEpithelial-Mesenchymal TransitionHypertension, PulmonaryLupus Erythematosus, SystemicPulmonary Arterial HypertensionTh17 CellsActivin Receptors, Type IIAdultAnimalsCoculture TechniquesEndothelial CellsEndothelial-Mesenchymal TransitionFemaleHumansInterleukin-17activin AActivin Receptors, Type IActivin Receptors, Type IIActivinsACVRL1 protein, humanInterleukin-17

Identifiers

PMID40395196
PMCPMC12569737

What OpenQuestion holds

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Registered trials

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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.