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| http://dx.doi.org/10.1172/jci.insight.145847 | DOI Listing |
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Induction of macrophage efferocytosis in pancreatic cancer via PI3Kγ inhibition and radiotherapy promotes tumour control.
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January 2025
Nuffield Department of Surgical Sciences, University of Oxford, Oxford, UK
Background: The immune suppression mechanisms in pancreatic ductal adenocarcinoma (PDAC) remain unknown, but preclinical studies have implicated macrophage-mediated immune tolerance. Hence, pathways that regulate macrophage phenotype are of strategic interest, with reprogramming strategies focusing on inhibitors of phosphoinositide 3-kinase-gamma (PI3Kγ) due to restricted immune cell expression. Inhibition of PI3Kγ alone is ineffective in PDAC, despite increased infiltration of CD8+ T cells.
View Article and Find Full Text PDFStaphylococcus aureus vesicles impair cutaneous wound healing through p38 MAPK-MerTK cleavage-mediated inhibition of macrophage efferocytosis.
Cell Commun Signal
January 2025
School of Pharmaceutical Sciences, Southern Medical University, Guangzhou, 510515, China.
Background: Staphylococcus aureus, a known contributor to non-healing wounds, releases vesicles (SAVs) that influence the delicate balance of host-pathogen interactions. Efferocytosis, a process by which macrophages clear apoptotic cells, plays a key role in successful wound healing. However, the precise impact of SAVs on wound repair and efferocytosis remains unknown.
View Article and Find Full Text PDFTumor initiating cells escape tumor immunity via CCL8 from tumor-associated macrophages in mice.
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Department of Medical Oncology; Department of Pancreato-Biliary Surgery; De, Center for Translational Medicine, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Tumor-initiating cells (TICs) play a key role in cancer progression and immune escape. However, how TICs evade immune elimination remains poorly characterized. Combining single-cell RNA sequencing (scRNA-seq), dual-recombinase-based lineage tracing, and other approaches, we identified a WNT-activated subpopulation of malignant cells that act as TICs in vivo.
View Article and Find Full Text PDFComprehensive analysis of scRNA-seq and bulk RNA-seq reveals the non-cardiomyocytes heterogeneity and novel cell populations in dilated cardiomyopathy.
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State Key Laboratory of Cardiovascular Diseases and Medical Innovation Center, School of Medicine, Shanghai East Hospital, Tongji University, Shanghai, 200120, China.
Background: Dilated cardiomyopathy (DCM) is one of the most common causes of heart failure. Infiltration and alterations in non-cardiomyocytes of the human heart involve crucially in the occurrence of DCM and associated immunotherapeutic approaches.
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A feeding-induced myokine modulates glucose homeostasis.
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January 2025
State Key Laboratory of Membrane Biology, MOE Key Laboratory of Bioinformatics, Tsinghua-Peking Center for Life Sciences, School of Life Sciences, Tsinghua University, Beijing, China.
Maintaining blood glucose homeostasis during fasting and feeding is crucial for the prevention of dysregulation that can lead to either hypo- or hyperglycaemia. Here we identified feimin, encoded by a gene with a previously unknown function (B230219D22Rik in mice, C5orf24 in humans), as a key modulator of glucose homeostasis. Feimin is secreted from skeletal muscle during feeding and binds to its receptor, receptor protein tyrosine kinase Mer (MERTK), promoting glucose uptake and inhibiting glucose production by activation of AKT.
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