Knockout of thyroid hormone receptor alpha a (thraa) enhances cardiac regeneration in zebrafish through metabolic and hypoxic regulation

Abstract Background Thyroid hormone (TH) signaling drives cardiomyocyte (CM) maturation in endothermic animals. Elevated TH levels, coupled with increased basal metabolism, promote CM cell cycle exit and polyploidization, thus limiting heart regenerative potential. However, a comprehensive understan...

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Main Authors: Man Yee Cheung, Chunmei Jiang, Imtiaz Ul Hassan, Hui Wang, Donghao Guo, Daniel Wuyang Dio, Huan Yan, Jianmin Sun, Xufeng Qi, Dongqing Cai, Wei Ge, Sheue-yann Cheng, Wai-Yee Chan, Hui Zhao
Format: Article
Language:English
Published: BMC 2025-07-01
Series:Cell Communication and Signaling
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Online Access:https://doi.org/10.1186/s12964-025-02350-5
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author Man Yee Cheung
Chunmei Jiang
Imtiaz Ul Hassan
Hui Wang
Donghao Guo
Daniel Wuyang Dio
Huan Yan
Jianmin Sun
Xufeng Qi
Dongqing Cai
Wei Ge
Sheue-yann Cheng
Wai-Yee Chan
Hui Zhao
author_facet Man Yee Cheung
Chunmei Jiang
Imtiaz Ul Hassan
Hui Wang
Donghao Guo
Daniel Wuyang Dio
Huan Yan
Jianmin Sun
Xufeng Qi
Dongqing Cai
Wei Ge
Sheue-yann Cheng
Wai-Yee Chan
Hui Zhao
author_sort Man Yee Cheung
collection DOAJ
description Abstract Background Thyroid hormone (TH) signaling drives cardiomyocyte (CM) maturation in endothermic animals. Elevated TH levels, coupled with increased basal metabolism, promote CM cell cycle exit and polyploidization, thus limiting heart regenerative potential. However, a comprehensive understanding of TH and its receptors, thyroid hormone receptors (TRs), orchestrating with other regulatory processes for heart regeneration, such as the hypoxia signaling pathway and post-injury metabolic switches, remains elusive. Results Here, we investigated the molecular mechanisms of TH signaling in heart regeneration using a time-course sequencing experiment. We assessed heart regeneration capacity in thyroid hormone receptor alpha a (thraa) mutant zebrafish, which carry an 8-bp insertion that leads to truncation of the Thraa protein and impaired TH signaling. The thraa + 8 bp mutant zebrafish exhibited an enhanced heart regenerative response. Our study showed that, in thraa +/– mutants, a transiently augmented inflammatory response and an extended CM proliferative window are associated with metabolic switches across different phases. Moreover, we found that thraa transcriptionally regulates hypoxia-inducible factor 3 subunit alpha (hif3a), and its knockout in zebrafish impairs heart regeneration. Conclusions In conclusion, our study highlights the role of TH signaling via thraa in modulating zebrafish heart regeneration through metabolic regulation, inflammation, cardiac tissue regeneration, and its interplay with hif3a.
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spelling doaj-art-35cc647d2f9c4debb418d893421326b22025-08-20T03:43:01ZengBMCCell Communication and Signaling1478-811X2025-07-0123112110.1186/s12964-025-02350-5Knockout of thyroid hormone receptor alpha a (thraa) enhances cardiac regeneration in zebrafish through metabolic and hypoxic regulationMan Yee Cheung0Chunmei Jiang1Imtiaz Ul Hassan2Hui Wang3Donghao Guo4Daniel Wuyang Dio5Huan Yan6Jianmin Sun7Xufeng Qi8Dongqing Cai9Wei Ge10Sheue-yann Cheng11Wai-Yee Chan12Hui Zhao13Key Laboratory for Regenerative Medicine, School of Biomedical Sciences, Faculty of Medicine, Ministry of Education, The Chinese University of Hong KongKey Laboratory for Regenerative Medicine, School of Biomedical Sciences, Faculty of Medicine, Ministry of Education, The Chinese University of Hong KongKey Laboratory for Regenerative Medicine, School of Biomedical Sciences, Faculty of Medicine, Ministry of Education, The Chinese University of Hong KongTranslational and Functional Genomics Branch, National Human Genome Research InstituteDivision of Cardiology, Renji Hospital, School of Medicine, Shanghai Jiao Tong UniversityKey Laboratory for Regenerative Medicine, School of Biomedical Sciences, Faculty of Medicine, Ministry of Education, The Chinese University of Hong KongKey Laboratory for Regenerative Medicine, School of Biomedical Sciences, Faculty of Medicine, Ministry of Education, The Chinese University of Hong KongDepartment of Pathogen Biology and Immunology, School of Basic Medical Sciences, Ningxia Medical UniversityKey Laboratory of Regenerative Medicine of Ministry of Education, Department of Developmental & Regenerative Biology, Jinan UniversityKey Laboratory of Regenerative Medicine of Ministry of Education, Department of Developmental & Regenerative Biology, Jinan UniversityDepartment of Biomedical Sciences and Centre of Reproduction, Development and Aging (CRDA), Faculty of Health Sciences, University of MacauLaboratory of Molecular Biology, National Cancer Institute, National Institutes of HealthKey Laboratory for Regenerative Medicine, School of Biomedical Sciences, Faculty of Medicine, Ministry of Education, The Chinese University of Hong KongKey Laboratory for Regenerative Medicine, School of Biomedical Sciences, Faculty of Medicine, Ministry of Education, The Chinese University of Hong KongAbstract Background Thyroid hormone (TH) signaling drives cardiomyocyte (CM) maturation in endothermic animals. Elevated TH levels, coupled with increased basal metabolism, promote CM cell cycle exit and polyploidization, thus limiting heart regenerative potential. However, a comprehensive understanding of TH and its receptors, thyroid hormone receptors (TRs), orchestrating with other regulatory processes for heart regeneration, such as the hypoxia signaling pathway and post-injury metabolic switches, remains elusive. Results Here, we investigated the molecular mechanisms of TH signaling in heart regeneration using a time-course sequencing experiment. We assessed heart regeneration capacity in thyroid hormone receptor alpha a (thraa) mutant zebrafish, which carry an 8-bp insertion that leads to truncation of the Thraa protein and impaired TH signaling. The thraa + 8 bp mutant zebrafish exhibited an enhanced heart regenerative response. Our study showed that, in thraa +/– mutants, a transiently augmented inflammatory response and an extended CM proliferative window are associated with metabolic switches across different phases. Moreover, we found that thraa transcriptionally regulates hypoxia-inducible factor 3 subunit alpha (hif3a), and its knockout in zebrafish impairs heart regeneration. Conclusions In conclusion, our study highlights the role of TH signaling via thraa in modulating zebrafish heart regeneration through metabolic regulation, inflammation, cardiac tissue regeneration, and its interplay with hif3a.https://doi.org/10.1186/s12964-025-02350-5Thyroid hormoneMetabolismHypoxiaHeart regenerationInflammationCardiomyocytes
spellingShingle Man Yee Cheung
Chunmei Jiang
Imtiaz Ul Hassan
Hui Wang
Donghao Guo
Daniel Wuyang Dio
Huan Yan
Jianmin Sun
Xufeng Qi
Dongqing Cai
Wei Ge
Sheue-yann Cheng
Wai-Yee Chan
Hui Zhao
Knockout of thyroid hormone receptor alpha a (thraa) enhances cardiac regeneration in zebrafish through metabolic and hypoxic regulation
Cell Communication and Signaling
Thyroid hormone
Metabolism
Hypoxia
Heart regeneration
Inflammation
Cardiomyocytes
title Knockout of thyroid hormone receptor alpha a (thraa) enhances cardiac regeneration in zebrafish through metabolic and hypoxic regulation
title_full Knockout of thyroid hormone receptor alpha a (thraa) enhances cardiac regeneration in zebrafish through metabolic and hypoxic regulation
title_fullStr Knockout of thyroid hormone receptor alpha a (thraa) enhances cardiac regeneration in zebrafish through metabolic and hypoxic regulation
title_full_unstemmed Knockout of thyroid hormone receptor alpha a (thraa) enhances cardiac regeneration in zebrafish through metabolic and hypoxic regulation
title_short Knockout of thyroid hormone receptor alpha a (thraa) enhances cardiac regeneration in zebrafish through metabolic and hypoxic regulation
title_sort knockout of thyroid hormone receptor alpha a thraa enhances cardiac regeneration in zebrafish through metabolic and hypoxic regulation
topic Thyroid hormone
Metabolism
Hypoxia
Heart regeneration
Inflammation
Cardiomyocytes
url https://doi.org/10.1186/s12964-025-02350-5
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