ArticleMolecular medicine reports2026
<p>Artemisiae Scopariae Herba (Yinchen) suppresses ferroptosis in mice with osteoporosis via the Nrf2/Slc7a11/Gpx4 pathway</p>.
Article in Molecular medicine reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
- Biological Activity ofInternational journal of molecular sciences · 2026Article
- Targeting ferroptosis in osteoporosis: mechanisms and natural products therapies.Frontiers in pharmacology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
<p>With the aging of the population, the incidence of postmenopausal osteoporosis (PMOP) is increasing. Extracts from Artemisiae Scopariae Herba, also known as Yinchen (YC), promote osteogenic differentiation and bone formation; however, the specific mechanism is unclear. The present study aimed to investigate the effects and mechanism of YC on PMOP. Ultra‑performance liquid chromatography‑tandem mass spectrometry was used to determine the potential predominant components of YC, and an ovariectomized (OVX) mouse model was established to evaluate the effects of YC on PMOP and its potential mechanisms. Initially, the therapeutic effect of YC on PMOP was assessed by micro‑CT bone analysis, pathological observation and ELISA detection. Combined with serum ELISA, reverse transcription‑quantitative PCR and immunohistochemical staining, the potential key anti‑PMOP pathway of YC was explored. A total of 2,072 compounds were identified in YC. The main active components of YC included chlorogenic acid, ferulic acid and caffeic acid. Experimental studies provided evidence that YC may improve bone loss and bone microstructure deterioration caused by ovariectomy. YC treatment also upregulated serum estrogen levels, and the expression of osteoprotegerin, runt‑related transcription factor 2 and glutathione peroxidase 4 (Gpx4) in bone tissue. Ovariectomy led to abnormal iron metabolism and increase the accumulation of lipid peroxides. YC reduced liver iron deposition, restored glutathione levels, and downregulated serum tartrate‑resistant acid phosphatase, osteocalcin, ferritin and hepcidin levels in mice. In addition, YC reversed the decreased expression of nuclear factor erythroid 2‑related factor 2 (Nrf2), solute carrier family 7 member 11 (Slc7a11) and Gpx4 in the bone tissues of OVX mice. In conclusion, the present study suggested the effectiveness of YC in potentially reducing ovariectomy‑induced osteoporosis in mice. YC promoted bone formation and improved bone microstructure, potentially by inhibiting ferroptosis via activation of the Nrf2/Slc7a11/Gpx4 pathway in OVX mice.</p>.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.