Evidence map›Paper›PMID 37111757›Full record

ArticlePharmaceutics2023

Human Salivary Histatin-1 Attenuates Osteoarthritis through Promoting M1/M2 Macrophage Transition.

Antong Wu, Janak Lal Pathak, Xingyang Li, Wei Cao, Wenchao Zhong, Mingjing Zhu, Qiuyu Wu, Wanyi Chen, Qiao Han, Siqing Jiang and 4 more

Open access · goldAbstract read
In one paragraph

Article in Pharmaceutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Exploring the Healing Powers of Histatins: From Oral Health to Therapeutics.International journal of molecular sciences · 2025
    Review
  5. Article
  6. Review
  7. Article
  8. Article
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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

14 authors at 2 institutions in 2 countries.

Antong WuDepartment of Temporomandibular Joint, Affiliated Stomatology Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou 510182, China.
Janak Lal PathakDepartment of Temporomandibular Joint, Affiliated Stomatology Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou 510182, China.ORCID 0000-0003-2576-443X
Xingyang LiDepartment of Temporomandibular Joint, Affiliated Stomatology Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou 510182, China.
Wei CaoDepartment of Temporomandibular Joint, Affiliated Stomatology Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou 510182, China.
Wenchao ZhongDepartment of Temporomandibular Joint, Affiliated Stomatology Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou 510182, China.
Mingjing ZhuDepartment of Temporomandibular Joint, Affiliated Stomatology Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou 510182, China.
Qiuyu WuGuangdong Engineering Research Center of Oral Restoration and Reconstruction, Guangzhou Key Laboratory of Basic and Applied Research of Oral Regenerative Medicine, Guangzhou 510182, China.
Wanyi ChenDepartment of Temporomandibular Joint, Affiliated Stomatology Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou 510182, China.
Qiao HanDepartment of Temporomandibular Joint, Affiliated Stomatology Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou 510182, China.
Siqing JiangDepartment of Temporomandibular Joint, Affiliated Stomatology Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou 510182, China.
Yuzhuo HeiDepartment of Temporomandibular Joint, Affiliated Stomatology Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou 510182, China.
Ziyi ZhangDepartment of Temporomandibular Joint, Affiliated Stomatology Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou 510182, China.
Gang WuDepartment of Oral and Maxillofacial Surgery/Pathology, Amsterdam UMC and Academic Center for Dentistry Amsterdam (ACTA), Vrije Universiteit Amsterdam (VU), Amsterdam Movement Science (AMS), 1081 LA Amsterdam, The Netherlands.ORCID 0000-0001-8941-2500
Qingbin ZhangDepartment of Temporomandibular Joint, Affiliated Stomatology Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou 510182, China.
Stomatology Hospital · CNAcademic Center for Dentistry Amsterdam · NL

Funding

Guangzhou Health Commission General Project 20191A010067Guangzhou Science and Technology Key R&D Program Fund 202206010004High-level university construction funding of Guangzhou Medical University 02-412-B205002-1003017 and 06-410-2106035Medical Science and Technology Research Foundation of Guangdong Province A202205National Natural Science Foundation of China 82150410451
6 · The paper itself

Abstract

Osteoarthritis (OA) is an inflammation-driven degenerative joint disease. Human salivary peptide histatin-1 (Hst1) shows pro-healing and immunomodulatory properties. but its role in OA treatment is not fully understood. In this study, we investigated the efficacy of Hst1 in the inflammation modulation-mediated attenuation of bone and cartilage damage in OA. Hst1 was intra-articularly injected into a rat knee joint in a monosodium iodoacetate (MIA)-induced OA model. Micro-CT, histological, and immunohistochemical analyses showed that Hst1 significantly attenuates cartilage and bone deconstruction as well as macrophage infiltration. In the lipopolysaccharide-induced air pouch model, Hst1 significantly reduced inflammatory cell infiltration and inflammation. Enzyme-linked immunosorbent assay (ELISA), RT-qPCR, Western blot, immunofluorescence staining, flow cytometry (FCM), metabolic energy analysis, and high-throughput gene sequencing showed that Hst1 significantly triggers M1-to-M2 macrophage phenotype switching, during which it significantly downregulated nuclear factor kappa-B (NF-κB) and mitogen-activated protein kinases (MAPK) signaling pathways. Furthermore, cell migration assay, Alcian blue, Safranin O staining, RT-qPCR, Western blot, and FCM showed that Hst1 not only attenuates M1-macrophage-CM-induced apoptosis and matrix metalloproteinase expression in chondrogenic cells, but it also restores their metabolic activity, migration, and chondrogenic differentiation. These findings show the promising potential of Hst1 in treating OA.

Indexed as

chondrogenic lineage cellshistatin-1macrophagesosteoarthritissynovium

Identifiers

PMID37111757
PMCPMC10147060
OpenAlexW4366425796

What OpenQuestion holds

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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.