DDAH1 (dimethylarginine dimethylaminohydrolase 1) is a critical metabolic enzyme that hydrolyzes asymmetric dimethylarginine (ADMA) and monomethyl-L-arginine (MMA), endogenous inhibitors of nitric oxide synthase (NOS) 1. By degrading these NOS inhibitors, DDAH1 promotes nitric oxide (NO) production and regulates vascular function and systemic blood pressure 1. The enzyme is essential for maintaining NO-mediated endothelial cell apoptosis and angiogenesis in pulmonary microvascular systems 1. Genetically, DDAH1 and DDAH2 are the primary determinants of circulating ADMA concentration, with SNP variants significantly affecting blood ADMA levels 2. Pathologically, DDAH1 plays diverse roles across multiple diseases: in cancer, tumor-secreted DDAH1 promotes lung fibrosis and aging via TGF-β1/Smad3 signaling 3, while elevated DDAH1 confers cisplatin chemoresistance in nasopharyngeal carcinoma through EGFR-JAK2-STAT3 pathway activation 4. Conversely, reduced DDAH1 expression associates with enhanced renal cell carcinoma proliferation and metastasis 5. In non-malignant conditions, DDAH1 dysfunction underlies polycystic ovary syndrome pathogenesis through ADMA accumulation and oxidative stress 6, and DDAH1 dysregulation contributes to addiction and social stress phenotypes via the ADMA-NOS axis 7. DDAH1 inhibition emerges as a therapeutic strategy in pathologies with excessive NO production 8.