{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nTNFRSF12A, commonly known as Fn14, is the exclusive cell‐surface receptor for the cytokine TWEAK and plays a pivotal role in normal tissue homeostasis and repair. In nonmalignant settings, Fn14 activation regulates cellular responses that are critical for tissue regeneration and inflammation. For instance, TWEAK–Fn14 signaling in skeletal muscle progenitor and mesenchymal stem cells promotes proliferation while inhibiting terminal differentiation, thereby facilitating muscle repair."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "3"}]}, {"type": "t", "text": " In addition, endothelial cells and vascular smooth muscle cells respond to TWEAK via Fn14 to induce pro‐inflammatory cytokine production and adhesion molecule expression, contributing to vascular remodeling and atherosclerotic progression."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": " Fn14 is also expressed on adipose tissue–derived mesenchymal cells, where its activation modulates adipogenesis, and its upregulation in renal and hepatic injury models has been linked to enhanced inflammatory mediator release and subsequent tissue remodeling."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "6", "end_ref": "17"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its role in normal repair, Fn14 is increasingly recognized as a driver of malignant progression. Elevated Fn14 expression has been documented in several human cancers—including glioblastoma, breast, prostate, esophageal, and non‐small cell lung cancers—where its activation promotes tumor cell migration, invasion, and resistance to apoptosis through NF‑κB–dependent upregulation of anti‐apoptotic molecules. In glioma models, for example, TWEAK–Fn14 engagement facilitates a positive feedback loop that further increases Fn14 expression and enhances invasive behavior, while in breast and prostate cancers, high Fn14 levels correlate with poor prognosis and metastatic propensity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "18", "end_ref": "38"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAt the molecular level, the TWEAK–Fn14 axis engages complex signaling cascades that modulate cell fate decisions and present promising therapeutic targets. Detailed structure–function studies have identified critical residues required for high‐affinity TWEAK binding"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "39"}]}, {"type": "t", "text": ", while kinetic analyses have underscored the impact of ligand multimerization on differential NF‑κB pathway activation."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "41"}]}, {"type": "t", "text": " Moreover, in disease contexts such as psoriasis and HPV‐associated lesions, aberrant Fn14 expression contributes to a switch from apoptosis to proliferation in keratinocytes"}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "42", "end_ref": "44"}]}, {"type": "t", "text": ", and evidence of TWEAK‐independent Fn14 self-association further expands its signaling repertoire."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "45"}]}, {"type": "t", "text": " These insights collectively emphasize the potential of targeting the TWEAK–Fn14 pathway to modulate inflammatory and malignant processes.\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Norihiro Harada, Masafumi Nakayama, Hiroyasu Nakano, et al. 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