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Nicotinamide mononucleotide restores impaired metabolism, endothelial cell proliferation and angiogenesis in old sedentary male mice.
iScience
January 2025
Department of Vascular Surgery, Lausanne University Hospital (CHUV), Lausanne, Switzerland.
Aging is accompanied by a decline in neovascularization potential and increased susceptibility to ischemic injury. Here, we confirm the age-related impaired neovascularization following ischemic leg injury and impaired angiogenesis. The age-related deficits in angiogenesis arose primarily from diminished EC proliferation capacity, but not migration or VEGF sensitivity.
View Article and Find Full Text PDFIFN-γ licenses normal and pathogenic ALPK1/TIFA pathway in human monocytes.
iScience
January 2025
CIRI, Centre International de Recherche en Infectiologie, Inserm U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, ENS de Lyon, University Lyon, F-69007 Lyon, France.
Alpha-kinase 1 (ALPK1) is an immune receptor sensing the bacterial nucleotide sugar ADP-heptose. ALPK1 phosphorylates TIFA leading to its oligomerization and downstream NF-κB activation. Specific mutations in are associated with an autoinflammatory syndrome termed ROSAH and with spiradenoma (skin cancers with sweat gland differentiation).
View Article and Find Full Text PDFA Novel COL7A1 Mutation in a Patient With Dystrophic Epidermolysis Bullosa. Successful Treatment With Upadacitinib.
Clin Cosmet Investig Dermatol
January 2025
Department of Dermatology, Candidate Branch of National Clinical Research Centre for Skin and Immune Diseases, First Affiliated Hospital of Gannan Medical University, Ganzhou, 341000, People's Republic of China.
Dystrophic epidermolysis bullosa (DEB) is a heterogeneous and rare genetic skin disease caused by mutations in the gene, which encodes Type VII collagen. The absence or dysfunction of Type VII collagen can cause the dense lower layer of the basal membrane zone of the skin to separate from the dermis, leading to blister formation and various complications. In different DEB subtypes, the severity of the phenotype is associated, to some extent, with the outcome of Type VII collagen caused by mutations in the gene, which may be reduced in expression, remarkably reduced, or completely absent.
View Article and Find Full Text PDFInfiltrating lipid-rich macrophage subpopulations identified as a regulator of increasing prostate size in human benign prostatic hyperplasia.
Front Immunol
January 2025
Division of Urology, Department of Surgery, Endeavor Health (formerly NorthShore University HealthSystem), Evanston, IL, United States.
Introduction: Macrophages exhibit marked phenotypic heterogeneity within and across disease states, with lipid metabolic reprogramming contributing to macrophage activation and heterogeneity. Chronic inflammation has been observed in human benign prostatic hyperplasia (BPH) tissues, however macrophage activation states and their contributions to this hyperplastic disease have not been defined. We postulated that a shift in macrophage phenotypes with increasing prostate size could involve metabolic alterations resulting in prostatic epithelial or stromal hyperplasia.
View Article and Find Full Text PDFCD56 CD16 cells represent a distinct mature NK cell subset with altered phenotype and are associated with adverse clinical outcome upon expansion in AML.
Front Immunol
January 2025
Team Immunity and Cancer, Cancer Research Center of Marseille (CRCM), Inserm U1068, CNRS UMR7258, Paoli-Calmettes Institute, University of Aix-Marseille UM105, Marseille, France.
Introduction: Acute myeloid leukemia (AML) is a rare haematological cancer with poor 5-years overall survival (OS) and high relapse rate. Leukemic cells are sensitive to Natural Killer (NK) cell mediated killing. However, NK cells are highly impaired in AML, which promote AML immune escape from NK cell immune surveillance.
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