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Peer-reviewedCC BYScientific Reports

Genomic structural equation modeling reveals a common genetic dimension contributing to variation in growth‑related traits across multiple developmental stages

  • Jiajun Chang1
  • Juan Chen1
  • Ziying Wu2
  • Aijing Xu2
  1. 1Longhua District Central Hospital of Shenzhen
  2. 2Department of Genetics and Endocrinology, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University
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Abstract

Adult height serves as a comprehensive biological proxy for early-life conditions and long-term well-being. Despite the well-established genetic basis of height, current research predominantly employs single-trait or timepoint-specific analyses, thereby limiting the systemic elucidation of the shared genetic architecture spanning from developmental initiation to structural maturation. We applied Genomic Structural Equation Modeling (Genomic SEM) to integrate large-scale GWAS summary statistics for five phenotypes: birth weight, IGF-1 levels, bone mineral density, childhood height, and adult height. Post-GWAS analyses included fine-mapping, TWAS with FOCUS, pathway enrichment, cell-type specificity, and spatial transcriptomic mapping. A single latent growth trait demonstrated excellent model fit (CFI = 0.996, SRMR = 0.028). Multivariate GWAS identified 2,120 independent lead variants, with fine-mapping prioritizing high-confidence causal variants at loci including ACAN, IHH, and ADAMTS17. Pathway enrichment converged on endochondral ossification and GH/IGF-1 signaling. Cell-type analysis revealed significant enrichment in mesenchymal lineages, while spatial mapping localized signals predominantly to the cartilage primordium. This study provides a unified genetic framework connecting early-life initiation, molecular mediation, and structural development, offering novel insights into the systemic developmental principles governing human height.

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Cite

BibTeXRIS
BibTeX
@article{chang2026genomic,
  title = {{Genomic structural equation modeling reveals a common genetic dimension contributing to variation in growth‑related traits across multiple developmental stages}},
  author = {Jiajun Chang and Juan Chen and Ziying Wu and Aijing Xu},
  journal = {Scientific Reports},
  year = {2026},
  month = jul,
  doi = {10.1038/s41598-026-63047-4},
  url = {https://doi.org/10.1038/s41598-026-63047-4},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Genomic structural equation modeling reveals a common genetic dimension contributing to variation in growth‑related traits across multiple developmental stages
AU  - Jiajun Chang
AU  - Juan Chen
AU  - Ziying Wu
AU  - Aijing Xu
PY  - 2026
DA  - 2026/07/01
JO  - Scientific Reports
DO  - 10.1038/s41598-026-63047-4
UR  - https://doi.org/10.1038/s41598-026-63047-4
AB  - Adult height serves as a comprehensive biological proxy for early-life conditions and long-term well-being. Despite the well-established genetic basis of height, current research predominantly employs single-trait or timepoint-specific analyses, thereby limiting the systemic elucidation of the shared genetic architecture spanning from developmental initiation to structural maturation. We applied Genomic Structural Equation Modeling (Genomic SEM) to integrate large-scale GWAS summary statistics for five phenotypes: birth weight, IGF-1 levels, bone mineral density, childhood height, and adult height. Post-GWAS analyses included fine-mapping, TWAS with FOCUS, pathway enrichment, cell-type specificity, and spatial transcriptomic mapping. A single latent growth trait demonstrated excellent model fit (CFI = 0.996, SRMR = 0.028). Multivariate GWAS identified 2,120 independent lead variants, with fine-mapping prioritizing high-confidence causal variants at loci including ACAN, IHH, and ADAMTS17. Pathway enrichment converged on endochondral ossification and GH/IGF-1 signaling. Cell-type analysis revealed significant enrichment in mesenchymal lineages, while spatial mapping localized signals predominantly to the cartilage primordium. This study provides a unified genetic framework connecting early-life initiation, molecular mediation, and structural development, offering novel insights into the systemic developmental principles governing human height.
SN  - 2045-2322
ER  -