Single-cell data revealed the function of natural killer cells and macrophage cells in chemotherapy tolerance in acute myeloid leukemia DOI Creative Commons
Jing Gao,

Xue-Qian Yan,

Dan Fan

и другие.

PeerJ, Год журнала: 2024, Номер 12, С. e18521 - e18521

Опубликована: Ноя. 21, 2024

Background Acute myeloid leukemia (AML) is highly prevalent and heterogeneous among adult acute leukemias. Current chemotherapeutic approaches for AML often face the challenge of drug resistance, immune cells play an important role in regulation resistance. Thus, it key significance to explore regulatory mechanisms alleviate chemotherapy resistance AML. Methods Based on single-cell transcriptomic data, this study revealed differences expression cell subpopulations marker genes patients complete remission group (CR) compared non-complete (non-CR) after chemotherapy. Functional enrichment by clusterprofiler functions differentially expressed (DEGs) AUCell scores were used assess immunoregulatory cells. Pseudotime analysis was construct differentiation trajectories. CellChat cellular communication elucidate interactions between Survival with R package “survival” prognosis. Finally, wound healing trans-well assay performed. Results Single-cell clustering that NK/T macrophage significantly higher non-CR than CR FCAR+ FCGR3A+ macrophages more active correlated processes regulating energy metabolism activity. Differentially NK groups mainly included HBA1 , S100A8 S100A9 which associated cancer regulation, these ( FCAR FCGR3A PREX1 ) upregulated human chronic (HAP1) silencing affected migration invasion HAP1 In particular, pathways differed from those group. Cellular analyses showed ligand-receptor pairs HLA-E-KLRK1, HLA-E-KLRC1, HLA-E-CD94:NKG2A, CLEC2B-KLRB1. addition, LGALS9-CD45, CCL3L1- CCR1, CCL3-CCR1 two regulate secreted signaling mediate progression. Marker Conclusion This reveals potential chemoresistance through RNA sequencing data. provides new ideas insights into treatment.

Язык: Английский

Regulated Cell death in Acute Myocardial Infarction: Molecular Mechanisms and Therapeutic Implications DOI
Lili Zhu,

Yiyang Liu,

Kangkai Wang

и другие.

Ageing Research Reviews, Год журнала: 2024, Номер 104, С. 102629 - 102629

Опубликована: Дек. 5, 2024

Язык: Английский

Процитировано

8

Single-Cell WGCNA Combined with Transcriptome Sequencing to Study the Molecular Mechanisms of Inflammation-Related Ferroptosis in Myocardial Ischemia-Reperfusion Injury DOI Creative Commons
Zhuohua Zhang, Yan Liu,

Da Huang

и другие.

Journal of Inflammation Research, Год журнала: 2024, Номер Volume 17, С. 6203 - 6227

Опубликована: Сен. 1, 2024

Myocardial ischemia-reperfusion injury (MIRI) is characterized by inflammation and ferroptosis, but the precise mechanisms remain unknown. This study used single-cell transcriptomics technology to investigate changes in various cell subtypes during MIRI regulatory network of ferroptosis-related genes immune infiltration.

Язык: Английский

Процитировано

4

Qing-Xin-Jie-Yu Granule attenuates myocardial infarction-induced inflammatory response by regulating the MK2/TTP pathway DOI Creative Commons

Jianghan Qi,

Xiaoyao Gao,

Ying Han

и другие.

Pharmaceutical Biology, Год журнала: 2025, Номер 63(1), С. 128 - 140

Опубликована: Фев. 21, 2025

Context Qing-Xin-Jie-Yu Granule (QXJYG) has shown promise in the treatment of myocardial infarction. However, mechanism action QXJYG underlying its anti-inflammation remain unknown.

Язык: Английский

Процитировано

0

Identification and validation of three diagnostic autophagy-related genes associated with advanced plaques and immune cell infiltration in carotid atherosclerosis based on integrated bioinformatics analyses DOI Creative Commons
Tengbo Huang, Su Chen, Qingjun Su

и другие.

PeerJ, Год журнала: 2024, Номер 12, С. e18543 - e18543

Опубликована: Ноя. 22, 2024

Autophagy plays a key role in the development of carotid atherosclerosis (CAS). This study aimed to identify autophagy-related genes (ATGs) related with CAS using bioinformatics analysis,

Язык: Английский

Процитировано

1

Single-cell data revealed the function of natural killer cells and macrophage cells in chemotherapy tolerance in acute myeloid leukemia DOI Creative Commons
Jing Gao,

Xue-Qian Yan,

Dan Fan

и другие.

PeerJ, Год журнала: 2024, Номер 12, С. e18521 - e18521

Опубликована: Ноя. 21, 2024

Background Acute myeloid leukemia (AML) is highly prevalent and heterogeneous among adult acute leukemias. Current chemotherapeutic approaches for AML often face the challenge of drug resistance, immune cells play an important role in regulation resistance. Thus, it key significance to explore regulatory mechanisms alleviate chemotherapy resistance AML. Methods Based on single-cell transcriptomic data, this study revealed differences expression cell subpopulations marker genes patients complete remission group (CR) compared non-complete (non-CR) after chemotherapy. Functional enrichment by clusterprofiler functions differentially expressed (DEGs) AUCell scores were used assess immunoregulatory cells. Pseudotime analysis was construct differentiation trajectories. CellChat cellular communication elucidate interactions between Survival with R package “survival” prognosis. Finally, wound healing trans-well assay performed. Results Single-cell clustering that NK/T macrophage significantly higher non-CR than CR FCAR+ FCGR3A+ macrophages more active correlated processes regulating energy metabolism activity. Differentially NK groups mainly included HBA1 , S100A8 S100A9 which associated cancer regulation, these ( FCAR FCGR3A PREX1 ) upregulated human chronic (HAP1) silencing affected migration invasion HAP1 In particular, pathways differed from those group. Cellular analyses showed ligand-receptor pairs HLA-E-KLRK1, HLA-E-KLRC1, HLA-E-CD94:NKG2A, CLEC2B-KLRB1. addition, LGALS9-CD45, CCL3L1- CCR1, CCL3-CCR1 two regulate secreted signaling mediate progression. Marker Conclusion This reveals potential chemoresistance through RNA sequencing data. provides new ideas insights into treatment.

Язык: Английский

Процитировано

0