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A novel LIPUS system was developed and evaluated in rat AKI models, focusing on its effects on glomerular filtration rate (GFR), blood urea nitrogen (BUN), serum creatinine (SCr), and the Notch1\u2010Akt\u2010eNOS signaling pathway. The results demonstrated that LIPUS treatment improved GFR, BUN, SCr levels, and renal pathology in AKI rats. In\u00a0vitro experiments using HUVEC cells revealed that LIPUS stimulation promoted angiogenesis, cell migration mechanically\u2010dependent calcium ion influx, which was partially attenuated by TRPV1 knockdown. RNA sequencing analysis indicated LIPUS\u2010induced activation of the Notch pathway, phosphorylation of Akt and eNOS. Furthermore, inhibition or genetic silencing of Notch1 abolished the beneficial effects of LIPUS on angiogenesis, renal function, and Akt\u2010eNOS phosphorylation in both cells and AKI rats. These findings suggest that LIPUS\u2010induced calcium influx promotes Akt\u2010eNOS phosphorylation, nitric oxide (NO) production, angiogenesis, and improved renal function in AKI via Notch1\u2010Akt\u2010eNOS signaling, positioning LIPUS as a promising therapeutic strategy for AKI by targeting vascular regeneration.<\/jats:p>","DOI":"10.1096\/fj.202401142rr","type":"journal-article","created":{"date-parts":[[2025,1,9]],"date-time":"2025-01-09T07:45:48Z","timestamp":1736408748000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Mechanosensitive Ca\n                    <sup>2+<\/sup>\n                    channel\n                    <scp>TRPV1<\/scp>\n                    activated by low\u2010intensity pulsed ultrasound ameliorates acute kidney injury through Notch1\u2010Akt\u2010\n                    <scp>eNOS<\/scp>\n                    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