ArticleMaterials today. Bio2026
Layered double hydroxide nanocarriers loaded with butylphthalide attenuate the AKI-CKD transition by regulating mitophagy.
Article in Materials today. Bio, 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
Acute kidney injury (AKI) caused by ischemia-reperfusion (IR) is an independent risk factor for the progression of chronic kidney disease (CKD), yet there is a lack of effective clinical interventions. Although butylphthalide (NBP) has been proven to have multi-organ protective potential, its rapid in vivo metabolism and low bioavailability limit its clinical application. To overcome these limitations, we rationally designed and synthesized a layered double hydroxide (LDHs)-based nanocarrier system for NBP delivery (LDHs@NBP) via hydrothermal co-precipitation. Comprehensive characterization confirmed successful nanocomplex formation. Critically, LDHs@NBP exhibited accelerated NBP release under mildly acidic conditions, matching the pathological acidosis of injured and fibrotic renal tubules-thereby achieving pH-responsive drug release. Using both an in vivo rat model of unilateral renal ischemia-reperfusion injury (uIRI) and an in vitro TGF-β1-stimulated HK-2 cell model, we demonstrated that LDHs@NBP significantly attenuated renal dysfunction, suppressed interstitial fibrosis, and improved mitochondrial function. Importantly, all protective effects were abolished upon co-treatment with Mdivi-1, confirming mitophagy as the central mechanistic axis. Collectively, this study successfully constructed LDHs@NBP nanocomplexes with pH-responsive drug release properties. This system enhances mitophagy by activating the PINK1-Parkin pathway, thereby effectively blocking AKI-CKD transition. It provides a new strategy with good translational prospects for clinical intervention in kidney diseases.
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