ArticleNeurospine2025
Vitamin A Deficiency Induces Congenital Vertebral Malformation via Retinoic Acid Signaling Mediated Sclerotome Dysplasia.
Article in Neurospine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Syndactyly in pigs.Open veterinary journal · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors.
Funding
Abstract
objectiveCongenital vertebral malformations (CVMs) arise from abnormal sclerotome development. Our previous study has indicated that vitamin A deficiency (VAD) induced congenital spinal deformity in rats. However, the phenotype observed through x-ray and the mechanism were still unclear.
methodsRats in VAD group were fed with a diet without added vitamin A, while rats in control group were fed with a normal diet. After mating, embryos were collected, and neonatal rats were euthanized. Micro-computed tomography and x-ray were utilized to detect the vertebral malformation. We applied whole mount in situ hybridization to visualize the expression patterns of Pax1 and Raldh-2 in embryos. Laser capture microdissection combined RNA-seq of sclerotome was performed.
resultsThe incidence of CVMs in neonatal rats was 32.65% in VAD group and 0% in control group. All malformations observed were butterfly vertebrae. In VAD group, we observed downregulation of Pax1 in sclerotome and Raldh-2 in somite. The enriched gene ontology terms were related to developmental process of skeletal system. The enriched pathways were related to osteoblast and osteoclast differentiation, somitogenesis, and retinol metabolism. Real-time quantitative polymerase chain reaction validated that retinoic acid (RA) signaling was downregulated in the sclerotome, leading to the suppression of osteoblast differentiation through a non-Smad-dependent bone morphogenetic protein (BMP) signaling pathway.
conclusionWe established a VAD-induced CVMs model. Non-Smad-dependent BMP pathway and RA signaling pathway may be related to the pathogenesis of CVMs. Our findings demonstrate that VAD may be one of the causes of CVMs, which is hypothesized to serve as a novel therapeutic target for the nonsurgical treatment of CVMs in the future.
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.