A Cardiac-Targeted Nanozyme Interrupts the Inflammation-Free Radical Cycle in Myocardial Infarction

© 2023 Wiley-VCH GmbH.

Détails bibliographiques
Publié dans:Advanced materials (Deerfield Beach, Fla.). - 1998. - 36(2024), 2 vom: 08. Jan., Seite e2308477
Auteur principal: Liu, Xueliang (Auteur)
Autres auteurs: Chen, Binghua, Chen, Jingqi, Wang, Xuan, Dai, Xinfeng, Li, Yuqing, Zhou, Huayuan, Wu, Lian-Ming, Liu, Zhuang, Yang, Yu
Format: Article en ligne
Langue:English
Publié: 2024
Accès à la collection:Advanced materials (Deerfield Beach, Fla.)
Sujets:Journal Article block of inflammation-free radical cycle cardiac targeting myocardial infarction nanozyme tannic acid Anti-Inflammatory Agents Free Radicals Polyphenols
Description
Résumé:© 2023 Wiley-VCH GmbH.
Severe systemic inflammation following myocardial infarction (MI) is a major cause of patient mortality. MI-induced inflammation can trigger the production of free radicals, which in turn ultimately leads to increased inflammation in cardiac lesions (i.e., inflammation-free radicals cycle), resulting in heart failure and patient death. However, currently available anti-inflammatory drugs have limited efficacy due to their weak anti-inflammatory effect and poor accumulation at the cardiac site. Herein, a novel Fe-CurTA nanozyme is developed for targeted therapy of MI, which is generated by coordinating Fe3+ and anti-inflammatory drug curcumin (Cur) with further modification of tannic acid (TA). Such Fe-Cur@TA nanozyme exhibits excellent free radicals scavenging and anti-inflammatory properties by reducing immune cell infiltration, promoting macrophage polarization toward the M2-like phenotype, suppressing inflammatory cytokine secretion, and blocking the inflammatory free radicals cycle. Furthermore, due to the high affinity of TA for cardiac tissue, Fe-Cur@TA shows an almost tenfold greater in cardiac retention and uptake than Fe-Cur. In mouse and preclinical beagle dog MI models, Fe-Cur@TA nanozyme preserves cardiac function and reduces scar size, suggesting promising potential for clinical translation in cardiovascular disease
Description:Date Completed 12.01.2024
Date Revised 03.01.2025
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-4095
DOI:10.1002/adma.202308477