Evidence map›Paper›PMID 39367607›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2024

Bone-protective effects of neutralizing angiopoietin-like protein 4 monoclonal antibody in rheumatoid arthritis.

Liqing Ke, Qifei He, Jing Qu, Xiyue Wang, Kaibo Li, Xun Gong, Lan Li, Jiake Xu, Qiuliyang Yu, Hao Yu and 7 more

Abstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2024. 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
–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

12 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. [Puerarin alleviates rheumatoid arthritis in rats by modulating TAK1-mediated TLR4/NF-κB signaling pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
    Article
  9. Article
  10. Article
  11. Review
  12. ANGPTL4-mediated inflammation: A new mechanism of disease and therapeutic approach for rheumatoid arthritis.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    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

17 authors.

Liqing KeShenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong 518055, China.
Qifei HeDepartment of Bone Joint and Musculoskeletal Tumor, Shenzhen Second People's Hospital (The First Affiliated Hospital of Shenzhen University), Shenzhen, Guangdong 518035, China.
Jing QuShenzhen Center for Disease Control and Prevention, Shenzhen, Guangdong 518055, China.
Xiyue WangShenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong 518055, China.
Kaibo LiShenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong 518055, China.
Xun GongGuang'anmen Hospital China Academy of Chinese Medical Sciences, Beijing 100053, China.
Lan LiDepartment of Pathology, Beijing Jishuitan Hospital, Capital Medical University, Beijing 100035, China.
Jiake XuShenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong 518055, China; Shenzhen University of Advanced Technology, Shenzhen, Guangdong 518060, China; School of Biomedical Sciences, University of Western Australia, Perth, WA 6009, Australia.
Qiuliyang YuShenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong 518055, China; Shenzhen University of Advanced Technology, Shenzhen, Guangdong 518060, China.
Hao YuShenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong 518055, China.
Xuefei LinShenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong 518055, China.
Jian LiShenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong 518055, China.
Nguan Soon TanLee Kong Chian School of Medicine, Nanyang Technological University Singapore, Singapore 308232, Singapore; School of Biological Sciences, Nanyang Technological University, Singapore 138673, Singapore.
Wei SunDepartment of Bone Joint and Musculoskeletal Tumor, Shenzhen Second People's Hospital (The First Affiliated Hospital of Shenzhen University), Shenzhen, Guangdong 518035, China.
Liang LiDepartment of Pharmacology, School of Medicine, Southern University of Science and Technology, Shenzhen, Guangdong 518055, China. Electronic address: lil@sustech.edu.cn.
Peng ZhangShenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong 518055, China; Shenzhen University of Advanced Technology, Shenzhen, Guangdong 518060, China; The Key Laboratory of Biomedical Imaging Science and System, Chinese Academy of Sciences, Shenzhen, Guangdong 518055, China; Shandong Zhongke Advanced Technology Co., Ltd., Jinan, Shandong 250300, China. Electronic address: peng.zhang@siat.ac.cn.
Wenxiang ChengShenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong 518055, China. Electronic address: wx.cheng@siat.ac.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite recent advances, rheumatoid arthritis (RA) patients remain refractory to therapy. Dysregulated overproduction of angiopoietin-like protein 4 (ANGPTL4) is thought to contribute to the disease development. ANGPTL4 was initially identified as a regulator of lipid metabolism, which is hydrolyzed to N-terminal and C-terminal (cANGPTL4) fragments in vivo. cANGPTL4 is involved in several non-lipid-related processes, including angiogenesis and inflammation. This study revealed that the level of ANGPTL4 was markedly elevated in the sera and synovial tissues from patients with RA versus controls. The administration of a neutralizing antibody against cANGPTL4 (anti-cANGPTL4 Ab) resulted in the inhibition of inflammatory processes and bone loss in animal models of collagen-induced arthritis and adjuvant-induced arthritis (AIA). Transcriptomic and proteomic profiling of synovial tissues from an AIA model indicated that the anti-cANGPTL4 Ab inhibited fibroblast-like synoviocyte (FLS) immigration and inflammatory-induced osteoclastogenesis. Mechanistically, the anti-cANGPTL4 Ab has been shown to inhibit TNF-α-induced inflammatory cascades in RA-FLS through the sirtuin 1/nuclear factor-κB signaling pathway. Moreover, the anti-cANGPTL4 Ab was found to block FLS invasion- and immigration-induced osteoclast activation. Collectively, these findings identify ANGPTL4 as a prospective biomarker for the diagnosis of RA, and targeting cANGPTL4 should represent a potential therapeutic strategy.

Indexed as

Angiopoietin-Like Protein 4Arthritis, RheumatoidAnimalsAntibodies, MonoclonalAntibodies, NeutralizingArthritis, ExperimentalBone and BonesDisease Models, AnimalFemaleHumansMaleMiceOsteoclastsOsteogenesisSignal TransductionSynovial MembraneAngiopoietin-Like Protein 4ANGPTL4 protein, humanAntibodies, MonoclonalAntibodies, NeutralizingANGPTL4biologic therapybone protectioninflammationrheumatoid arthritis

Identifiers

PMID39367607
PMCPMC11638830

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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.