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10.1186/s12987-025-00637-w http://scihub22266oqcxt.onion/10.1186/s12987-025-00637-w C11959998!11959998!40170044     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=40170044&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\40170044.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Fluids+Barriers+CNS 2025 ; 22 (ä): ä Nephropedia Template TP {{tp|p=40170044|t=2025. Brain endothelial cells as phagocytes: mechanisms and implications |pdf=|usr=}}{{40170044}} gab.com Text Brain endothelial cells as phagocytes: mechanisms and implications JO: Fluids Barriers CNS http://www.kidney.de/pget.php?&tw=1&pmid=40170044 #FOAvip Brain microvascular endothelial cells (BECs) lining the brain capillaries form the anatomical site of the blood-brain barrier (BBB), providing a highly selective barrier to support brain homeostasis and function. While the BBB acts as a barrier to immune cells and pathogens under normal conditions, BECs can facilitate their entry into the CNS via a phagocytosis-like mechanism. A similar process is now increasingly reported for a diverse set of cargos, resulting in the categorization of BECs as ?non-professional? phagocytes and redefining the conventional view that these cells are functionally non-phagocytic. This review aims to summarize research demonstrating the capacity of BECs to phagocytose various cargos, including aged red blood cells (RBC), myelin debris, and embolic particles. Mechanistically, BEC phagocytosis can be triggered by the exposure of phosphatidylserine on RBC, expression of adhesion molecules such as ICAM-1 and VCAM-1 on BECs, cargo-opsonization, and/or involve BEC cytoskeleton remodeling. Phagocytic activity by BECs has significant clinical implications ranging from regulation of cerebral microvascular patency (particularly by contributing to and resolving capillary stalling), clearance of brain parenchymal debris, and brain parenchymal invasion by pathogens. Further, BEC phagocytosis of RBC, which represents a cell (RBC)-in-cell (BEC) phenomenon, is implicated in hemorrhagic lesions including cerebral microhemorrhages. This review aims to shed light on BEC phagocytosis as an important function within the brain microvascular system and will delve into the underlying mechanisms, discuss the clinical implications, and identify gaps in our understanding of this phenomenon. Twit Text FOAVip Brain endothelial cells as phagocytes: mechanisms and implications ????Fluids Barriers CNS http://www.kidney.de/pget.php?&tw=1&pmid=40170044 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=40170044 #FOAvip English Wikipedia <ref>{{Cite pmid|40170044}}</ref> Brain endothelial cells as phagocytes: mechanisms and implications #MMPMID40170044 Chang RT; Fisher MJ; Sumbria RK Fluids Barriers CNS 2025[]; 22 (ä): ä PMID40170044show ga Brain microvascular endothelial cells (BECs) lining the brain capillaries form the anatomical site of the blood-brain barrier (BBB), providing a highly selective barrier to support brain homeostasis and function. While the BBB acts as a barrier to immune cells and pathogens under normal conditions, BECs can facilitate their entry into the CNS via a phagocytosis-like mechanism. A similar process is now increasingly reported for a diverse set of cargos, resulting in the categorization of BECs as ?non-professional? phagocytes and redefining the conventional view that these cells are functionally non-phagocytic. This review aims to summarize research demonstrating the capacity of BECs to phagocytose various cargos, including aged red blood cells (RBC), myelin debris, and embolic particles. Mechanistically, BEC phagocytosis can be triggered by the exposure of phosphatidylserine on RBC, expression of adhesion molecules such as ICAM-1 and VCAM-1 on BECs, cargo-opsonization, and/or involve BEC cytoskeleton remodeling. Phagocytic activity by BECs has significant clinical implications ranging from regulation of cerebral microvascular patency (particularly by contributing to and resolving capillary stalling), clearance of brain parenchymal debris, and brain parenchymal invasion by pathogens. Further, BEC phagocytosis of RBC, which represents a cell (RBC)-in-cell (BEC) phenomenon, is implicated in hemorrhagic lesions including cerebral microhemorrhages. This review aims to shed light on BEC phagocytosis as an important function within the brain microvascular system and will delve into the underlying mechanisms, discuss the clinical implications, and identify gaps in our understanding of this phenomenon. äBrain endothelial cells as phagocytes: mechanisms and implications (epmc).pdf DeepDyve Pubget Overpricing