{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nPDCD10, also known as CCM3, was originally identified as a causative gene for cerebral cavernous malformations (CCMs)—a group of vascular lesions characterized by abnormally dilated, hemorrhage‐prone capillaries in the central nervous system. Loss‐of‐function mutations in PDCD10 disrupt vascular morphogenesis and remodeling by impairing apoptosis and endothelial cell function, thereby contributing to both familial and sporadic forms of CCM. These observations, derived from molecular genetic analyses and mutation‐screening studies, underscore the critical role of PDCD10 in maintaining vascular integrity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "7"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAt the molecular level, PDCD10 functions as an intracellular adaptor protein that participates in numerous protein–protein interactions essential for endothelial signaling. It physically associates with CCM2 and directly binds several kinases—including STK25, MST4, and other members of the germinal center kinase III (GCKIII) family—and interacts with proteins such as paxillin via its focal adhesion targeting (FAT)–homology domain. Through these interactions, PDCD10 modulates several signaling pathways including ERK1/2, MAPK, and PI3K cascades, thereby influencing Golgi apparatus organization, exocytosis (notably of angiopoietin-2), tight junction assembly, and overall endothelial barrier properties. In addition, PDCD10 participates in oxidative stress responses by promoting the phosphorylation of ERM proteins and further integrates signals from the DLL4–Notch pathway—crucial for proper angiogenesis—as well as regulating EphB4 forward signaling."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "8", "end_ref": "26"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its vascular functions, PDCD10 is increasingly recognized as a regulator in diverse pathological contexts, including tumorigenesis. Altered PDCD10 expression has been linked to enhanced cell proliferation, migration, and survival in various cancers such as non–small cell lung cancer, retinoblastoma, T-cell lymphoma, and glioblastoma. In these settings, PDCD10 expression is frequently modulated by microRNAs and circular RNAs (for example, miR-103, miR-181b, miR-222-3p, and miR-126), thereby impacting downstream pathways that govern epithelial–mesenchymal transition, angiogenesis, and the tumor microenvironment. Moreover, recent evidence connects PDCD10 dysfunction to defective autophagy, impaired senescence, and even a gut–brain signaling axis that may exacerbate CCM severity. Collectively, these findings reveal a multifaceted role for PDCD10 in orchestrating both endothelial homeostasis and oncogenic signaling, with important implications for novel therapeutic strategies."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "27", "end_ref": "42"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "F Bergametti, C Denier, P Labauge, et al. 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