ArticleNature aging2026
Cancer-cell-secreted DDAH1 induces TGF-β1/Smad3 signaling pathway to promote fibrosis and aging in lung.
Article in Nature aging, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Prognostic performance of Asian Working Group for Sarcopenia 2025 Constructs for activities of daily living at discharge after stroke: a head-to-head validation.European geriatric medicine · 2026Article
- Mitochondrial dysfunction in peri-implantitis: bioinformatics and machine learning analysis with in vivo experiment.Odontology · 2026Article
- Calcium Overloading-Induced UBE2O Upregulation Alleviates Neuronal Apoptosis.Molecular neurobiology · 2026Article
- Extracellular Vesicles as Dynamic Sensors of Redox-Inflammatory Balance: Potential Implications for Aging in Healthy Subjects.Biomedicines · 2026Article
- Muscle loss must be interpreted in the context of fluid imbalance: a dual-parameter model predicts functional outcomes after acute stroke.European geriatric medicine · 2026Article
- BMAL1 attenuates myocardial infarction-induced fibrosis via suppressing p-SMAD3/SMAD3 in TGF-β1 pathway.Biochemistry and biophysics reports · 2026Article
- Metabolic Crosstalk Between Host and Tumor as a Circuit of Resilience in Cancer Therapy.Cells · 2026Review
- TGF-β1 induces epithelial-mesenchymal transition and fibrosis of ureteral epithelial cells via targeting RACK1 in ureteropelvic junction obstruction.Translational pediatrics · 2026Article
- Putative identification of CASTOR1 as one of the targets of ganoderic acid a via thermal proteome profiling and molecular docking.Frontiers in pharmacology · 2026Article
- Lineage tracing reveals KSPFrontiers in cell and developmental biology · 2026Article
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
Lung aging is a multifactorial series of molecular alterations that leads to gradual deterioration of lung function and increased vulnerability to cancer. Tumor communicates with host organs partially through extracellular vesicles; however, the mechanistic drivers and consequences of lung aging in the context of cancer remain unclear. Here we identify cancer cell-secreted dimethylarginine dimethylaminohydrolase-1 (DDAH1) protein induces citrulline accumulation and promotes lung fibrosis and aging. Mechanistically, our single-cell sequencing and genetic knockout mice evidence that citrulline availability elevation inhibits peptidyl arginine deiminase 4-mediated transforming growth factor-β1 (TGF-β1) citrullination, thereby inducing the TGF-β1/Smad3 signaling pathway in lung fibroblasts. Notably, vacuolar protein sorting assists the packaging of DDAH1 into the late endosomes. The administration of DDAH1 inhibitor reduces fibrosis and alleviates lung aging. Conclusively, our findings reveal tumor-derived DDAH1 protein contributes to citrulline accumulation to promote lung aging, shedding light on the treatment and diagnosis of tumors by inhibiting senescent lung fibroblasts.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.