Peritoneal dialysis (PD) can be used as renal replacement therapy when chronic kidney disease (CKD) progresses to end-stage renal disease. However, peritoneal fibrosis (PF) is a major cause of PD failure. Studies have demonstrated that PD fluid contains a significantly larger numbers of macrophages compared with the healthy individuals. During PD, macrophages can secrete cytokines to keep peritoneal tissue in sustained low-grade inflammation, and participate in the regulation of fibrosis-related signaling pathways, such as NF-κB, TGF-β/Smad, IL4/STAT6, and PI3K/AKT. A series of basic pathological changes occurs in peritoneal tissues, including epithelial mesenchymal transformation, overgeneration of neovasculature, and abnormal deposition of extracellular matrix. This review focuses on the role of macrophages in promoting PF during PD, summarizes the targets of macrophage-related inhibition of fibrosis, and provides new ideas for clinical research on delaying PF, maintaining the function and integrity of peritoneum, prolonging duration of PD as a renal replacement modality, and achieving longer survival in CKD patients.
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http://dx.doi.org/10.1080/0886022X.2025.2474203 | DOI Listing |
Hepatology
March 2025
Department of Liver Surgery and Transplantation, Liver Cancer Institute and Zhongshan Hospital, Fudan University, Shanghai, China.
Background And Aims: Portal vein tumor thrombosis (PVTT), an indicator of clinical metastasis, significantly shortens hepatocellular carcinoma (HCC) patients' lifespan, and no effective treatment has been established. We aimed to illustrate mechanisms underlying PVTT formation and tumor metastasis, and identified potential targets for clinical intervention.
Approach And Results: Multi-omics data of 159 HCC patients (including 37 cases with PVTT) was analyzed to identify contributors to PVTT formation and tumor metastasis.
J Immunol
January 2025
Program in Cell Biology, The Hospital for Sick Children, Toronto, ON, Canada.
Macrophages are important mediators of immune responses with critical roles in the recognition and clearance of pathogens, as well as in the resolution of inflammation and wound healing. The neuronal guidance cue SLIT2 has been widely studied for its effects on immune cell functions, most notably directional cell migration. Recently, SLIT2 has been shown to directly enhance bacterial killing by macrophages, but the effects of SLIT2 on inflammatory activation of macrophages are less known.
View Article and Find Full Text PDFSci Transl Med
March 2025
Clinical Neuroscience Research Center, Department of Neurosurgery and Neurology, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Traumatic brain injury (TBI) rapidly triggers proinflammatory activation of microglia, contributing to secondary brain damage post-TBI. Although the governing role of energy metabolism in shaping the inflammatory phenotype and function of immune cells has been increasingly recognized, the specific alterations in microglial bioenergetics post-TBI remain poorly understood. Itaconate, a metabolite produced by the enzyme aconitate decarboxylase 1 [IRG1; encoded by immune responsive gene 1 ()], is a pivotal metabolic regulator in immune cells, particularly in macrophages.
View Article and Find Full Text PDFJ Immunol
February 2025
Department of Biomedical and Molecular Sciences, Queen's University, Kingston, ON, Canada.
Endometriosis is a chronic disorder in which endometrial-like tissue presents outside the uterus. Patients with endometriosis have been shown to exhibit aberrant immune responses within the lesion microenvironment and in circulation which contribute to the development of endometriosis. Thymic stromal lymphopoietin (TSLP) is an alarmin involved in cell proliferation and the induction of T helper 2 (Th2) inflammation in various diseases, such as asthma, atopic dermatitis, and pancreatic and breast cancer.
View Article and Find Full Text PDFJ Immunol
March 2025
INSERM U1015, Gustave Roussy Cancer Campus, 114 rue Edouard Vaillant, Villejuif, 94805, France.
Microglia, the major population of brain resident macrophages, differentiate from yolk sac progenitors in the embryo and play multiple nonimmune roles in brain organization throughout development and life. Various microglia subtypes have been described by transcriptomic and proteomic signatures, involved metabolic pathways, morphology, intracellular complexity, time of residency, and ontogeny, both in development and in disease settings. Such macrophage heterogeneity increases with aging or neurodegeneration.
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