Tomentosin suppressed M1 polarization via increasing MERTK activation mediated by regulation of GAS6

Di, Yuxi; Bao, Yu-Jie; Zhu, Zhi-Qi; Sun, Shan-Liang; Tian, Feng-Xiang; Wang, Furong; Yu, Gui; Zhang, Ming-Fei; Han, Jian; Zhou, Lingling

doi:10.1016/j.jep.2023.116429

Cited by 5 publications

(1 citation statement)

References 32 publications

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“…The above genes were related to tissueresident macrophage. [25][26][27] Macrophage3 expressed a high level of ITGAX (Figure S5A), thus denoted a subset of proinflammatory macrophage. 28 HLA-DRA, which marked antigen-presenting cells, was found in macrophage5 (Figure S5A).…”

Section: Identifying Difference Of Macrophages In 3 Groupsmentioning

confidence: 99%

Overexpression of ATP5F1A in Cardiomyocytes Promotes Cardiac Reverse Remodeling

Xu,

Zhang,

Chang

et al. 2024

Circ: Heart Failure

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BACKGROUND: The mechanism of cardiac reverse remodeling (CRR) mediated by the left ventricular assist device remains unclear. This study aims to identify the specific cell type responsible for CRR and develop the therapeutic target that promotes CRR. METHODS: The nuclei were extracted from the left ventricular tissue of 4 normal controls, 4 CRR patients, and 4 no cardiac reverse remodeling patients and then subjected to single-nucleus RNA sequencing for identifying key cell types responsible for CRR. Gene overexpression in transverse aortic constriction and dilated cardiomyopathy heart failure mouse model (C57BL/6J background) and pathological staining were performed to validate the results of single-nucleus RNA sequencing. RESULTS: Ten cell types were identified among 126 156 nuclei. Cardiomyocytes in CRR patients expressed higher levels of ATP5F1A than the other 2 groups. The macrophages in CRR patients expressed more anti-inflammatory genes and functioned in angiogenesis. Endothelial cells that elevated in no cardiac reverse remodeling patients were involved in the inflammatory response. Echocardiography showed that overexpressing ATP5F1A through cardiomyocyte-specific adeno-associated virus 9 demonstrated an ability to improve heart function and morphology. Pathological staining showed that overexpressing ATP5F1A could reduce fibrosis and cardiomyocyte size in the heart failure mouse model. CONCLUSIONS: The present results of single-nucleus RNA sequencing and heart failure mouse model indicated that ATP5F1A could mediate CRR and supported the development of therapeutics for overexpressing ATP5F1A in promoting CRR.

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