ArticleAnimal models and experimental medicine2026
Ac-SDKP modulates apoptosis via HSP27 and the FAS/FASL and mitochondrial axes.
Article in Animal models and experimental 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
backgroundSilicosis is a progressive, irreversible fibrotic lung disease caused by long-term exposure to crystalline silica. Although the anti-fibrotic tetrapeptide Ac-SDKP has shown promise in reducing fibrosis, the specific molecular mechanisms through which it modulates apoptosis in silica-induced lung injury remain unclear, particularly the role of heat shock protein 27 (HSP27).
methodsWistar rats were divided into groups including control, model (2-week, 3-week, and 4-week), and Ac-SDKP prevention/treatment groups. In vitro, MEF and A549 cells were treated with TGF-β1 and Ac-SDKP to observe the effects on apoptosis-related proteins. Additionally, HSP27 interference vectors were constructed to study its role in regulating apoptosis via FAS/FASL and mitochondrial pathways in both in vivo and in vitro models.
resultsIn vivo, Ac-SDKP administration alleviated silica-induced pulmonary fibrosis and reduced apoptosis in lung tissue. In contrast, in vitro, TGF-β1 stimulation suppressed apoptosis in A549 and MEF cells, whereas Ac-SDKP restored apoptotic activity by regulating the HSP27-mediated FAS/FASL and mitochondrial pathways. Moreover, AAV9-mediated knockdown of HSP27 in mice enhanced apoptosis and attenuated fibrosis, confirming the anti-apoptotic role of HSP27 in silicosis.
conclusionThese findings reveal that Ac-SDKP exerts context-dependent modulation of apoptosis through HSP27-protecting acutely injured alveolar epithelial cells in vivo while reinstating apoptotic signaling in EMT-adapted A549 and MEF cells in vitro. Thus, targeting HSP27 may offer a promising therapeutic strategy to restore apoptotic-fibrotic equilibrium in silicosis and related pulmonary fibrotic disorders.
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