Author Correction: Embryological cellular origins and hypoxia-mediated mechanisms in PIK3CA-Driven refractory vascular malformations
Sota Torii, Keiki Nagaharu, Nanako Nakanishi, Hidehito Usui, Yumiko Hori, Katsutoshi Hirose, Satoru Toyosawa, Eiichi Morii, Mitsunaga Narushima, Yoshiaki Kubota, Osamu Nakagawa, Kyoko Imanaka-Yoshida, Kazuaki Maruyama
Abstract
Genes, proteins, chemicals, diseases, species, mutations and cell lines named across the full text — each resolved to its canonical identifier and authoritative record.
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Taxonomy
TopicsVascular Malformations Diagnosis and Treatment
Correction to: EMBO Molecular Medicine (2025). 10.1038/s44321-025-00235-1 | Published online 16 April 2025
The Synopsis bullet point list is corrected.
From:
- Phosphatase DUSP22 was identified as a regulator of skeletal muscle atrophy and treatment with the small molecule BML-260 produced therapeutic effects in multiple models of muscle wasting.
- DUSP22 gene knockdown or BML-260 treatment suppressed activation of the stress kinase JNK and its downstream target FOXO3a, which is a master regulator of muscle wasting.
- In aged skeletal muscle, DUSP22 gene knockdown reduced wasting-related gene expression by >50% and BML-260 therapy increased grip strength by >20%.
- These results demonstrate that the DUSP22-JNK-FOXO3a axis may be utilized to treat sarcopenia or related muscle wasting disorders and BML-260 can be an attractive lead compound for further drug development.
To:
- A mouse model was developed to mimic PIK3CAH1047R-driven vascular malformations restricted to the head and neck.
- Single-cell RNA-seq revealed significant upregulation of hypoxia pathways, including HIF-1α stabilization and VEGF-A expression.
- HIF-1α and VEGF-A inhibition reduced abnormal vessel growth, suggesting a potential therapeutic approach for refractory lesions.