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TIMD4-MHCⅡ巨噬细胞通过Retnla维持心脏功能。

TIMD4MHCⅡ Macrophages Preserve Heart Function Through Retnla.

作者信息

Zhang Danyang, Wang Xuanhao, Zhu Lianlian, Chen Yuxing, Yang Chao, Zhong Zhiwei, Kong Xiangming, Nan Jinliang, Wang Chen, Hu Hengxun, Chen Jinghai, Shi Peng, Hu Xinyang, Zhu Wei, Wang Jian'an

机构信息

Department of Cardiology, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.

State Key Laboratory of Transvascular Implantation Devices, Hangzhou, Zhejiang, China.

出版信息

JACC Basic Transl Sci. 2024 Nov 6;10(1):65-84. doi: 10.1016/j.jacbts.2024.08.009. eCollection 2025 Jan.

DOI:10.1016/j.jacbts.2024.08.009
PMID:39906591
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11788475/
Abstract

Genetic fate mapping confirmed the existence of the TIMD4MHCⅡ macrophage subset and showed that they were resident macrophages with minimal input from peripheral monocytes. Further, single-cell RNA sequencing revealed that could serve as the signature gene for TIMD4MHCⅡ macrophages. Administration of recombinant protein of the gene, RELMα, delayed the onset of heart failure, whereas either deletion of TIMD4MHCⅡ macrophages or macrophage-specific loss of facilitated heart failure progression.

摘要

遗传命运图谱证实了TIMD4MHCⅡ巨噬细胞亚群的存在,并表明它们是驻留巨噬细胞,外周单核细胞的输入极少。此外,单细胞RNA测序显示, 可作为TIMD4MHCⅡ巨噬细胞的特征基因。给予该基因的重组蛋白RELMα可延迟心力衰竭的发作,而删除TIMD4MHCⅡ巨噬细胞或巨噬细胞特异性缺失 则会促进心力衰竭的进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b55/11788475/03bc188f5c44/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b55/11788475/ff91c7c1de63/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b55/11788475/93bea77cf735/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b55/11788475/a6cd48a0b939/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b55/11788475/2a641f7153c1/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b55/11788475/d1eb0de3156c/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b55/11788475/2d828d02744b/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b55/11788475/9544aba76ef0/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b55/11788475/03bc188f5c44/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b55/11788475/ff91c7c1de63/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b55/11788475/93bea77cf735/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b55/11788475/a6cd48a0b939/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b55/11788475/2a641f7153c1/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b55/11788475/d1eb0de3156c/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b55/11788475/2d828d02744b/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b55/11788475/9544aba76ef0/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b55/11788475/03bc188f5c44/gr7.jpg

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Efferocytosis induces macrophage proliferation to help resolve tissue injury.
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Cell Metab. 2021 Dec 7;33(12):2445-2463.e8. doi: 10.1016/j.cmet.2021.10.015. Epub 2021 Nov 15.
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Cardiac Resident Macrophages Prevent Fibrosis and Stimulate Angiogenesis.心肌 Resident 巨噬细胞可预防纤维化并刺激血管生成。
Circ Res. 2021 Dec 3;129(12):1086-1101. doi: 10.1161/CIRCRESAHA.121.319737. Epub 2021 Oct 14.
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