ArticleBMC musculoskeletal disorders2021
Upregulated expression of transforming growth factor-β receptor I/II in an endemic Osteoarthropathy in China.
Article in BMC musculoskeletal disorders, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled 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.
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
3 citing papers in PubMed, 1 synthesis or guideline pooled it, 6 citations in OpenAlex.
- The efficacy of medial patellofemoral ligament reconstruction combined with distal femoral varus osteotomy in recurrent patellar dislocation and genu valgum.Musculoskeletal surgery · 2025Pooled it
- Transcriptome-wide RNA m6A methylation profiles in an endemic osteoarthropathy, Kashin-Beck disease.Journal of cellular and molecular medicine · 2024Article
- Induced pluripotent stem cells in cartilage tissue engineering: a literature review.Bioscience reports · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundKashin-Beck disease (KBD) is a chronic, deforming, endemic osteochondropathy that begins in patients as young as 2-3 years of age. The pathogenesis of KBD remains unclear, although selenium (Se) deficiency and T-2 toxin food contamination are both linked to the disease. In the present study, we evaluated transforming growth factor-β receptor (TGF-βR I and II) levels in clinical samples of KBD and in pre-clinical disease models.
methodsHuman specimens were obtained from the hand phalanges of eight donors with KBD and eight control donors. Animal models of the disease were established using Sprague-Dawley rats, which were fed an Se-deficient diet for 4 weeks and later administered the T-2 toxin. Cartilage cellularity and morphology were examined by hematoxylin and eosin staining. Expression and localization of TGF-βRI and II were evaluated using immunohistochemical staining and western blotting.
resultsIn the KBD samples, chondral necrosis was detected based on cartilage cell disappearance and alkalinity loss in the matrix ground substance. In the necrotic areas, TGF-βRI and II staining were strong. Positive percentages of TGF-βRI and II staining were higher in the cartilage samples of KBD donors than in those of control donors. TGF-βRI and II staining was also increased in cartilage samples from rats administered T-2 toxin or fed on Se-deficient plus T-2 toxin diets.
conclusionTGF-βRI and II may be involved in the pathophysiology of KBD. This study provides new insights into the pathways that contribute to KBD development.
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.