Triiodothyronine induces a proinflammatory monocyte/macrophage profile and impedes cardiac regeneration

IF 4.9 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Journal of molecular and cellular cardiology Pub Date : 2024-04-10 DOI:10.1016/j.yjmcc.2024.04.007

Ziwei Chen , Dongcheng Cai , Yifan Xie , Jiajun Zhong , Mengge Wu , Huijun Yang , Jie Feng , Hong Lian , Kefei Dou , Yu Nie

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Abstract

Neonatal mouse hearts can regenerate post-injury, unlike adult hearts that form fibrotic scars. The mechanism of thyroid hormone signaling in cardiac regeneration warrants further study. We found that triiodothyronine impairs cardiomyocyte proliferation and heart regeneration in neonatal mice after apical resection. Single-cell RNA-Sequencing on cardiac CD45-positive leukocytes revealed a pro-inflammatory phenotype in monocytes/macrophages after triiodothyronine treatment. Furthermore, we observed that cardiomyocyte proliferation was inhibited by medium from triiodothyronine-treated macrophages, while triiodothyronine itself had no direct effect on the cardiomyocytes in vitro. Our study unveils a novel role of triiodothyronine in mediating the inflammatory response that hinders heart regeneration.

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三碘甲状腺原氨酸会诱导单核细胞/巨噬细胞产生促炎作用，阻碍心脏再生

新生小鼠的心脏可以在损伤后再生，这与形成纤维化疤痕的成人心脏不同。甲状腺激素信号在心脏再生中的作用机制值得进一步研究。我们发现，三碘甲状腺原氨酸会损害心尖切除术后新生小鼠的心肌细胞增殖和心脏再生。心脏 CD45 阳性白细胞的单细胞 RNA 序列测定显示，三碘甲状腺原氨酸处理后，单核细胞/巨噬细胞具有促炎表型。此外，我们还观察到三碘甲腺原氨酸处理过的巨噬细胞培养基抑制了心肌细胞的增殖，而三碘甲腺原氨酸本身在体外对心肌细胞没有直接影响。我们的研究揭示了三碘甲腺原氨酸在介导炎症反应、阻碍心脏再生方面的新作用。

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来源期刊

Journal of molecular and cellular cardiology 医学-细胞生物学

CiteScore

10.70

自引率

0.00%

发文量

171

审稿时长

42 days

期刊介绍： The Journal of Molecular and Cellular Cardiology publishes work advancing knowledge of the mechanisms responsible for both normal and diseased cardiovascular function. To this end papers are published in all relevant areas. These include (but are not limited to): structural biology; genetics; proteomics; morphology; stem cells; molecular biology; metabolism; biophysics; bioengineering; computational modeling and systems analysis; electrophysiology; pharmacology and physiology. Papers are encouraged with both basic and translational approaches. The journal is directed not only to basic scientists but also to clinical cardiologists who wish to follow the rapidly advancing frontiers of basic knowledge of the heart and circulation.