Evidence map›Paper›PMID 32532031›Full record

ArticleInternational journal of molecular sciences2020

Effect of Angiotensin II on Bone Erosion and Systemic Bone Loss in Mice with Tumor Necrosis Factor-Mediated Arthritis.

Takahiko Akagi, Tomoyuki Mukai, Takafumi Mito, Kyoko Kawahara, Shoko Tsuji, Shunichi Fujita, Haruhito A Uchida, Yoshitaka Morita

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.3field-weighted citation impact, top 10% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Salt-Sensitive Hypertension Induces Osteoclastogenesis and Bone ResorptionFrontiers in cell and developmental biology · 2022
    Article
  8. TRAPS mutations inFrontiers in immunology · 2022
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Research of Pathogenesis and Novel Therapeutics in Arthritis 2.0.International journal of molecular sciences · 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

8 authors at 2 institutions in 1 country.

Takahiko AkagiDepartment of Rheumatology, Kawasaki Medical School, Kurashiki, Okayama 701-0192, Japan.
Tomoyuki MukaiDepartment of Rheumatology, Kawasaki Medical School, Kurashiki, Okayama 701-0192, Japan.ORCID 0000-0002-0103-1621
Takafumi MitoDepartment of Rheumatology, Kawasaki Medical School, Kurashiki, Okayama 701-0192, Japan.
Kyoko KawaharaDepartment of Rheumatology, Kawasaki Medical School, Kurashiki, Okayama 701-0192, Japan.
Shoko TsujiDepartment of Rheumatology, Kawasaki Medical School, Kurashiki, Okayama 701-0192, Japan.
Shunichi FujitaDepartment of Rheumatology, Kawasaki Medical School, Kurashiki, Okayama 701-0192, Japan.
Haruhito A UchidaDepartment of Chronic Kidney Disease and Cardiovascular Disease, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama 700-0914, Japan.ORCID 0000-0002-7629-7678
Yoshitaka MoritaDepartment of Rheumatology, Kawasaki Medical School, Kurashiki, Okayama 701-0192, Japan.ORCID 0000-0002-8000-0881
Kawasaki Medical School · JPOkayama University · JP

Funding

JSPS KAKENHI 20K08814Kawasaki Medical School R01-060 and 30-051UCB Japan N/A
6 · The paper itself

Abstract

Angiotensin II (Ang II) is the main effector peptide of the renin-angiotensin system (RAS), which regulates the cardiovascular system. The RAS is reportedly also involved in bone metabolism. The upregulation of RAS components has been shown in arthritic synovial tissues, suggesting the potential involvement of Ang II in arthritis. Accordingly, in the present study, we investigated the role of Ang II in bone erosion and systemic bone loss in arthritis. Ang II was infused by osmotic pumps in tumor necrosis factor-transgenic (TNFtg) mice. Ang II infusion did not significantly affect the severity of clinical and histological inflammation, whereas bone erosion in the inflamed joints was significantly augmented. Ang II administration did not affect the bone mass of the tibia or vertebra. To suppress endogenous Ang II, Ang II type 1 receptor (AT1R)-deficient mice were crossed with TNFtg mice. Genetic deletion of AT1R did not significantly affect inflammation, bone erosion, or systemic bone loss. These results suggest that excessive systemic activation of the RAS can be a risk factor for progressive joint destruction. Our findings indicate an important implication for the pathogenesis of inflammatory bone destruction and for the clinical use of RAS inhibitors in patients with rheumatoid arthritis.

Indexed as

Angiotensin IIAnimalsArthritis, ExperimentalBone ResorptionCancellous BoneFemaleInflammationJointsMaleMice, KnockoutMice, TransgenicReceptor, Angiotensin, Type 1Tumor Necrosis Factor-alphaX-Ray MicrotomographyAngiotensin IIReceptor, Angiotensin, Type 1TNF protein, humanTumor Necrosis Factor-alphaangiotensin IIangiotensin II type 1 receptorarthritisbone erosioninflammationrenin-angiotensin systemtumor necrosis factor

Identifiers

PMID32532031
PMCPMC7312645
OpenAlexW3035051154

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.