Evidence map›Paper›PMID 37189204›Full record

ArticleChinese medicine2023

Tanshinone IIA inhibits osteoclastogenesis in rheumatoid arthritis via LDHC-regulated ROS generation.

Qiuwei Peng, Jian Wang, Man Han, Minghong Zhao, Kesong Li, Tianming Lu, Qiuyan Guo, Quan Jiang

Open access · goldAbstract read
In one paragraph

Article in Chinese medicine, 2023. 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
3.7field-weighted citation impact, top 7% 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, 24 citations in OpenAlex.

  1. Glucose metabolism in osteoporosis: A potential therapeutic target (Review).International journal of molecular medicine · 2026
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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 3 institutions in 1 country.

Qiuwei Peng *Department of Rheumatology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, 100053, China.
Jian Wang *Department of Rheumatology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, 100053, China.
Man Han *Department of Rheumatology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, 100053, China.
Minghong ZhaoThe First School of Clinical Medicine, Gannan Medical University, Ganzhou, 341000, China.
Kesong LiDepartment of Rheumatology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, 100053, China.
Tianming LuSchool of Public Health, Guangxi Medical University, Guangxi, 530021, China.
Qiuyan GuoArtemisnin Research Center, and Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing, 100700, China. qyguo@icmm.ac.cn.ORCID http://orcid.org/0000-0002-0575-0105
Quan JiangDepartment of Rheumatology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, 100053, China. jiang.quan@hotmai.com.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNGannan Medical University · CNGuangxi Medical University · CN

Funding

CACMS Innovation Fund CI2021A01503Fundamental Research Funds for the Central public welfare research institutes ZZ13-YQ-033-C1Fundamental Research Funds for the Central public welfare research institutes ZZ14-YQ-060Fundamental Research Funds for the Central public welfare research institutes ZZ16-ND-10-9National Natural Science Foundation of China 82104480National Natural Science Foundation of China 82230121Scientific and Technological Innovation Project of Chinese Academy of Traditional Chinese Medicine CI2021A01511Young Elite Scientists Sponsorship Program by CACM 2021QNRC2B29
6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is characterized by bone destruction in the afflicted joints, and during the process of bone destruction, osteoclasts play a crucial role. Tanshinone IIA (Tan IIA) has shown anti-inflammatory effects in RA. However, the exact molecular mechanisms by which it delays bone destruction remain largely unexplained. Here, we found that Tan IIA decreased the severity of and ameliorated bone loss in an AIA rat model. In vitro, Tan IIA inhibited RANKL-induced osteoclast differentiation. By activity-based protein analysis (ABPP) combined with LC‒MS/MS, we discovered that Tan IIA covalently binds to the lactate dehydrogenase subunit LDHC and inhibits its enzymatic activity. Moreover, we found that Tan IIA inhibits the generation of osteoclast-specific markers by reducing the accumulation of reactive oxygen species (ROS), thus reducing osteoclast differentiation. Finally, our results reveal that Tan IIA suppresses osteoclast differentiation via LDHC-mediated ROS generation in osteoclasts. Tan IIA can thus be regarded as an effective drug for the treatment of bone damage in RA.

Indexed as

Lactate dehydrogenaseOsteoclastReactive oxygen speciesRheumatoid arthritisTanshinone IIA

Identifiers

PMID37189204
PMCPMC10184368
OpenAlexW4376610547

What OpenQuestion holds

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LicenceCC BY
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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.