Ultrasmall Polyphenol-NAD+ Nanoparticle-Mediated Renal Delivery for Mitochondrial Repair and Anti-Inflammatory Treatment of AKI-to-CKD Progression
© 2024 Wiley‐VCH GmbH.
Publié dans: | Advanced materials (Deerfield Beach, Fla.). - 1998. - 36(2024), 30 vom: 31. Juli, Seite e2310731 |
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Auteur principal: | |
Autres auteurs: | , , , , , , , , , , , , , , |
Format: | Article en ligne |
Langue: | English |
Publié: |
2024
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Accès à la collection: | Advanced materials (Deerfield Beach, Fla.) |
Sujets: | Journal Article acute kidney injury chronic kidney disease inflammation mitochondria nanoparticle nicotinamide adenine dinucleotide NAD 0U46U6E8UK Polyphenols plus... |
Résumé: | © 2024 Wiley‐VCH GmbH. As a central metabolic molecule, nicotinamide adenine dinucleotide (NAD+) can potentially treat acute kidney injury (AKI) and chronic kidney disease (CKD); however, its bioavailability is poor due to short half-life, instability, the deficiency of targeting, and difficulties in transmembrane transport. Here a physiologically adaptive gallic acid-NAD+ nanoparticle is designed, which has ultrasmall size and pH-responsiveness, passes through the glomerular filtration membrane to reach injured renal tubules, and efficiently delivers NAD+ into the kidneys. With an effective accumulation in the kidneys, it restores renal function, immune microenvironment homeostasis, and mitochondrial homeostasis of AKI mice via the NAD+-Sirtuin-1 axis, and exerts strong antifibrotic effects on the AKI-to-CKD transition by inhibiting TGF-β signaling. It also exhibits excellent stability, biodegradable, and biocompatible properties, ensuring its long-term safety, practicality, and clinical translational feasibility. The present study shows a potential modality of mitochondrial repair and immunomodulation through nanoagents for the efficient and safe treatment of AKI and CKD |
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Description: | Date Completed 25.07.2024 Date Revised 25.07.2024 published: Print-Electronic Citation Status MEDLINE |
ISSN: | 1521-4095 |
DOI: | 10.1002/adma.202310731 |