Gremlin1 repression-mediated mitochondrial network hyperfunction contributes to TCE-induced zebrafish cardiac defects
These results suggested that TCE-induced gremlin1 repression could result in mitochondrial hyperfunction, thereby hampering cardiomyocyte development and causing cardiac defects in zebrafish embryos. This study not only provided a novel insight into the etiology for environmental stressor-caused cardiac development defects, but also offered a potential therapeutic and preventive target for TCE-induced CHD.
Authors
- Tiantian Xia
- Huifang Deng (ORCID: https://orcid.org/0000-0002-1643-8205)
- Yue Gao (ORCID: https://orcid.org/0000-0001-6330-7171)
- Chaoji Huangfu (ORCID: https://orcid.org/0000-0002-8650-7149)
- Miao Chen (ORCID: https://orcid.org/0000-0002-1424-9160)
- Ningning Wang (ORCID: https://orcid.org/0000-0002-2820-4094)
- Li Zhang (ORCID: https://orcid.org/0000-0003-1092-7531)
- Wei Zhou (ORCID: https://orcid.org/0000-0002-9936-3789)
- Xiang Tang (ORCID: https://orcid.org/0000-0002-6843-7407)
- Ting Ao (ORCID: https://orcid.org/0000-0001-7070-3383)
- Congshu Huang
- Pan Shen
- Gaofu Li
- Zhijie Bai
Institutions
- Shenzhen Pingle Orthopedic Hospital (CN)
Publication Details
- Journal
- Cell Communication and Signaling
- Published
- 2025-07-01
- DOI
- https://doi.org/10.1186/s12964-025-02314-9
- Citations
- 1
- Primary Topic
- Congenital heart defects research
- Type
- article
- Field-Weighted Citation Impact
- 0.81