[Role of the TGF-β1 signaling pathway in modulating in vivo adaptation of vascular grafts].

Intimal hyperplasia and pseudoaneurysm formation after vascular graft implantation are key factors affecting long-term graft patency. The transforming growth factor-beta 1 (TGF-β1) signaling pathway, through Smad-dependent and non-Smad pathways, differentially regulates smooth muscle cell phenotypic switching and proliferation, shapes the immune-inflammatory microenvironment, influences the quality of the re-endothelialization process, and maintains the balance between extracellular matrix synthesis and degradation, thereby playing a central role in the occurrence and progression of graft stenosis and pseudoaneurysm. A spatiotemporal regulatory strategy that locally inhibits excessive activation of this pathway during the inflammatory and proliferative phases, while moderately enhancing its signaling during the remodeling and maturation phase to promote matrix homeostasis, may provide new ideas for the simultaneous prevention and treatment of restenosis and pseudoaneurysm. At present, intervention approaches such as local sustained-release systems, functional modification of tissue-engineered vessels, and gene and nucleic acid therapeutics are gradually being translated into clinical practice, aiming to achieve precise spatiotemporal regulation of TGF-β1 signaling. Future studies need to further integrate single-cell and spatial multi-omics technologies to elucidate patient heterogeneity in TGF-β1 signaling and to focus on developing intelligent, responsive biomaterials capable of sensing and dynamically intervening in the activity of this pathway, ultimately realizing individualized, time-sequenced therapy and promoting a shift in vascular grafts management from anatomical repair toward an integrated model of functional and structural restoration.