{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSPARCL1 is a secreted matricellular protein that modulates extracellular matrix organization and cell–cell adhesion, thereby influencing neural development and adult brain function. In the central nervous system it contributes to astroglial differentiation, regulates synaptogenesis, and is implicated in neuronal migration—processes essential for proper circuit formation. Altered SPARCL1 expression has been associated with neuropsychiatric disorders such as schizophrenia, with its dysregulation potentially affecting neuron–glia interactions, and with neurodegenerative conditions including Alzheimer’s disease and traumatic brain injury. Furthermore, studies in glaucoma and in alcohol use disorder indicate that SPARCL1 can interact with other ECM proteins and cell‐surface receptors to modulate synaptic stability and stress resilience."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "13"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn cancer settings, SPARCL1 is frequently downregulated or epigenetically silenced, and such loss correlates with enhanced tumor cell migration, invasion, and metastasis. In prostate, colorectal, renal, lung, and gastrointestinal stromal as well as esophageal and breast cancers, reduced SPARCL1 expression has been linked to poorer differentiation, increased metastatic potential, and worse clinical outcomes. In some tumor microenvironments—such as in colorectal carcinomas and high‐grade gliomas—SPARCL1 expression is associated with vascular stabilization and restricted focal adhesion assembly, suggesting that it functions as an endogenous inhibitor of malignancy. Together, these studies support a tumor‐suppressive role for SPARCL1 and raise the possibility of its use as a prognostic biomarker as well as a therapeutic target."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "14", "end_ref": "35"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nSPARCL1 also plays roles in vascular homeostasis and inflammatory responses. In cardiovascular contexts, elevated SPARCL1 levels have been observed in maladapted right ventricles in pulmonary hypertension and appear to serve as a biomarker for pathological remodeling. In addition, endothelial SPARCL1 overexpression can promote inflammatory cascades—as evidenced in experimental lung injury models—by acting on toll‐like receptor pathways and enhancing pro‐inflammatory macrophage phenotypes; alterations in its expression may thus impact both tissue repair and injury responses."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "36", "end_ref": "38"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its neural and oncologic functions, SPARCL1 is critical for extracellular matrix remodeling and influences developmental and reproductive processes. In non‐neural tissues such as the dermis, SPARCL1 (hevin) regulates collagen fibrillogenesis and decorin levels, thereby affecting wound healing and tissue mechanics. In the context of embryo implantation, SPARCL1 modulates trophoblast cell migration and invasion, suggesting a role in the establishment of early pregnancy. Emerging evidence in reproductive cancers further implicates SPARCL1 in mediating pathways controlled by microRNAs."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "39", "end_ref": "41"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Yanxia Li, J Daniel Aroca-Aguilar, Sikha Ghosh, et al. 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