{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSurfactant protein B (SP‐B), encoded by the SFTPB gene, is absolutely essential for normal lung function. Produced by alveolar type II pneumocytes as a 42‐kDa precursor that is proteolytically cleaved into an 8‐kDa mature peptide, SP‐B is critical for organizing and packaging surfactant phospholipids into lamellar bodies and for promoting the rapid adsorption of these lipids to the air–liquid interface. Structural and biophysical studies have shown that amphipathic domains within SP‐B facilitate membrane fusion, lipid mixing and lytic activities that lower alveolar surface tension, thereby preventing collapse at the end of expiration. Such findings highlight the indispensable role of SP‐B in surfactant metabolism and alveolar stability."}, {"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": "\nGenetic investigations have revealed that mutations and polymorphisms in SFTPB are strongly linked to a broad spectrum of pulmonary disorders. Variants in the SP‐B gene—including alterations in intronic regulatory elements and coding substitutions such as the Thr131Ile change—are associated with severe neonatal respiratory distress syndrome (RDS), interstitial lung disease, acute respiratory distress syndrome (ARDS) and chronic obstructive pulmonary disease (COPD), as well as with susceptibility to pneumonia and even heart failure–related lung injury. Such genetic variation can perturb SP‐B synthesis, processing and secretion, resulting in partial or complete deficiencies that compromise surfactant function and alveolar stability, thereby predisposing to lung injury and adverse clinical outcomes in diverse patient populations."}, {"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": "\nIn addition to genetic defects, SP‐B expression is finely regulated by diverse molecular signals and is modifiable by external factors. Transcriptional regulation mediated by factors such as thyroid transcription factor‑1—with modulation by TGF‑β/SMAD pathways—and the inhibitory effects of mediators like ceramide can markedly influence SP‐B levels, while pharmacological agents (for example, glucocorticoids and caffeine) have been demonstrated to synergistically increase SP‐B expression. Moreover, alterations in SP‐B levels in body fluids have been proposed as sensitive markers of lung injury, and emerging evidence even implicates SP‐B in influencing cellular responses to environmental or therapeutic stress, such as radiotherapy in lung cancer. These observations underscore the dynamic regulation of SP‐B in pulmonary biology and its potential as a therapeutic target in lung diseases."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "36", "end_ref": "40"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "R Haataja, M Rämet, R Marttila, et al. 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