ArticleJournal of nanobiotechnology2026
Degradable MMP9-responsive high-density lipoprotein nanoparticles enable efficient siRNA-PGRN and quercetin delivery to remodel the fibrotic microenvironment and attenuate renal fibrosis.
Article in Journal of nanobiotechnology, 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
Renal fibrosis is the final common pathway of chronic kidney disease and remains a challenge due to the complex fibrotic and inflammatory microenvironment. This study aimed to develop an enzyme-responsive, fibrosis-targeted nanotherapeutic system capable of simultaneously delivering siRNA against progranulin (siPGRN) and quercetin (QT) to remodel the fibrotic microenvironment and effectively attenuate renal fibrosis. The TIMP-HDL-Nano@siPGRN&QT nanoparticles prepared in this study exhibit uniform nanoscale size (~ 100 nm), high encapsulation efficiency, excellent stability, and favorable biocompatibility. The MMP9-responsive modification significantly enhanced renal accumulation and fibrotic lesion targeting in vivo. Treatment with TIMP-HDL-Nano@siPGRN&QT markedly alleviated UUO-induced renal injury, apoptosis, and fibrosis, outperforming free drug. Transcriptomic and mechanistic analyses revealed that the therapeutic effects were mediated through disruption of the PGRN-PPARα interaction, restoration of PPARα signaling, and subsequent inhibition of NF-κB-driven inflammatory pathways. Furthermore, the nanoparticles suppressed pro-inflammatory M1 macrophage polarization and promoted M2 polarization in a PPARα-dependent manner. This study demonstrates that TIMP-HDL-Nano@siPGRN&QT enables efficient, targeted co-delivery of siRNA and small-molecule therapeutics to fibrotic kidneys. By remodeling the fibrotic immune microenvironment through the PGRN-PPARα-NF-κB axis, this nanoplatform provides a potent and mechanistically defined strategy for the treatment of renal fibrosis and offers translational potential for other inflammation-driven fibrotic diseases.
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