Discussion

In summary, SIRT1 can participate in various physiological processes to alleviate stress-induced vascular senescence induced by irritants through multiple effector molecules and signaling pathways, in which “TP53” and “SOD” are among the top 20 molecules involved in oxidative stress (Figure 4), while “IL4,” “VCAM1,” “IL1B,” “IL10,” and other molecules rank among the top 20 in the inflammatory response process (Figure 5), suggesting that the SIRT1 protein can help improve stress-induced vascular senescence through antioxidant and anti-inflammatory effects. Meanwhile, molecules such as “AKT,” “TP53,” “HIF1A,” “MAPK,” “NRF2,” “FOXO1,” and “FOXO3” can interact with SIRT1 (Figure 2), indicating that SIRT1 is also involved in regulating autophagy, cell proliferation, and other processes and that it alleviates stress-induced vascular senescence.

This review offers a novel, network-guided synthesis of SIRT1-mediated regulation in stress-induced vascular senescence, setting it apart from previous reviews of SIRT1 and stress-induced vascular senescence. By integrating STRING/Cytoscape protein-interaction network analysis with a systematic pathway summary focused specifically on stress-driven premature stress-induced vascular senescence, rather than general aging or atherosclerosis, we prioritize mechanistic nodes with the strongest functional links to senescence phenotypes. This work provides an actionable, evidence-weighted framework for interpreting context-dependent SIRT1 signaling and identifying high-priority targets for future intervention in stress-induced vascular senescence.