Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
The choroid, which provides vascular supply to the outer retina, demonstrates progressive degeneration in aging and age-related macular degeneration (AMD). However mechanisms that maintain or compromise choroidal homeostasis are obscure. We discovered that the ablation of choroidal macrophages via CSF1R blockade was associated with choroidal vascular atrophy and retinal pigment epithelial (RPE) changes including structural disruption, downregulation of visual cycle genes, and altered angiogenic factor expression. Suspending CSF1R blockade following ablation enabled spontaneous macrophage regeneration, which fully restored original macrophage distributions and morphologies. Macrophage regeneration was accompanied by arrested vascular degeneration and ameliorated pathological RPE alterations. These findings suggest that choroidal macrophages play a previously unappreciated trophic role in maintaining choroidal vasculature and RPE cells, implicating insufficiency in choroidal macrophage function as a factor in aging- and AMD-associated pathology. Modulating macrophage function may constitute a strategy for the therapeutic preservation of the choroid and RPE in age-related retinal disorders.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7156269 | PMC |
| http://dx.doi.org/10.7554/eLife.55564 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Non-redundant immune checkpoints direct therapeutic resistance to chemoimmunotherapy in pancreatic ductal adenocarcinoma.
Cancer Immunol Res
September 2025
University of Pennsylvania, Philadelphia, PA, United States.
Pancreatic ductal adenocarcinoma (PDA) is defined by a myeloid-enriched microenvironment and has shown remarkable resistance to immune checkpoint blockade (e.g., PD-1 and CTLA-4).
View Article and Find Full Text PDFMonocytes are key circulating effectors of vascular homeostasis, innate immunity and inflammation. Following their generation in mouse bone marrow, classical (Ly6C ) monocytes are mobilized into the blood circulation where they mature into non-classical (Ly6C ) patrolling monocytes or are recruited into peripheral tissues where they differentiate into tissue resident or inflammatory macrophages. Monocytes and macrophages express CSF1R (CD115), the receptor for lineage-specific growth factors CSF1 and IL34.
View Article and Find Full Text PDFDeciphering spatially confined immune evasion niches in osteosarcoma with 3-D spatial transcriptomics: a literature review.
Front Oncol
July 2025
Department of Orthopedics, The Affiliated Hospital of Southwest Medical University, Luzhou, China.
Osteosarcoma (OS) is the most common primary malignant bone tumour of childhood, yet five-year survival has plateaued at ~60-70% for localised disease and plunges below 30% once metastasis emerges. Formerly viewed as a cell-intrinsic neoplasm entombed in mineralised bone, OS is now understood as a spatially stratified ecosystem whose immune-evasion niches choreograph progression. Three-dimensional spatial transcriptomics (3-D ST) fuses barcode-based transcript capture with volumetric reconstruction, preserving x-, y- and z-axis context and exposing concentric C1QC necrotic belts, MCAM (melanoma cell-adhesion molecule, CD146) peri-vascular corridors, hypoxic glycolytic rims and therapy-induced tertiary-lymphoid islets that collectively sequester cytotoxic lymphocytes.
View Article and Find Full Text PDFDual targeting of VEGFR2 and CSF1R with SYHA1813 confers novel strategy for treating both BRAF wild-type and mutant melanoma.
Cancer Cell Int
July 2025
Zhongshan Institute for Drug Discovery, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Zhongshan, 528400, China.
Background: Melanoma is notorious for its aggressive growth, metastatic spread, and heterogeneous response to therapy across BRAF (B-Raf proto-oncogene, serine/threonine kinase) genotypes. While BRAF inhibitors improve outcomes in V600E-mutant tumors, their benefit is limited in wild-type melanomas and by transient responses in mutant disease. Vascular endothelial growth factor receptor 2 (VEGFR2) driven angiogenesis and colony-stimulating factor-1 receptor (CSF1R) mediated immunosuppression each sculpt a permissive tumor microenvironment.
View Article and Find Full Text PDFAnti-CSF-1R therapy with combined immuno- chemotherapy coordinate an adaptive immune response to eliminate macrophage enriched Triple Negative Breast Cancers.
bioRxiv
May 2025
Department of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX, 77030, USA.
Patients diagnosed with metastatic triple negative breast cancer (mTNBC) have limited treatment options, are more prone to develop resistance and are associated with high mortality. A cold tumor immune microenvironment (TIME) characterized by low T cells and high tumor associated macrophages (TAMs) in mTNBC is associated with the failure of standard-of-care chemotherapy and immune checkpoint blockade (ICB) treatment. We demonstrate that the combination of immunomodulatory metronomic Cyclophosphamide (CTX) coupled with anti-CSF-1R antibody targeted therapy (SNDX-ms6352) and anti-PD-1 (ICB), was highly effective against aggressive metastatic syngeneic null TNBC genetically engineered mouse models (GEMMs) that present with high macrophage infiltration.
View Article and Find Full Text PDF