ArticleInternational journal of molecular medicine2026
Sirt1 attenuates calcific aortic valve disease by inhibiting ferroptosis and enhancing mitochondrial function via the activation of the Nrf2/HO‑1/FTH1 axis.
Article in International journal of molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Calcific aortic valve disease (CAVD) is a progressive disorder characterized by valvular calcification and currently lacks effective pharmacological therapies. Sirtuin 1 (Sirt1) has emerged as a cardioprotective factor; however, its role in CAVD remains unclear. The present study aimed to investigate whether Sirt1 attenuates CAVD by regulating iron homeostasis, ferroptosis and mitochondrial function through the nuclear factor erythroid 2‑related factor 2 (Nrf2)/heme oxygenase‑1 (HO‑1)/ferritin heavy chain 1 (FTH1) signaling axis. Sirt1 expression was evaluated in human calcified and non‑calcified aortic valves. Primary human aortic valve interstitial cells (hAVICs) were transfected with pcDNA3.1‑Sirt1 and subjected to osteogenic induction with or without the Nrf2 inhibitor, ML385, or the ferroptosis inducer, erastin. Osteogenic differentiation, mitochondrial function, ferroptosis and Nrf2/HO‑1/FTH1 signaling were analyzed.
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