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Advancements in nanomedicine for modulating ischemic cardiomyopathy therapy.

作者信息

Ren Xiangyi, Wang Yan, Yang Jian, Zhu Mengli, Zhang Ling, Li Lin

机构信息

Core Facilities of West China Hospital, Sichuan University, Chengdu, 610041, China.

Med-X Center for Materials, College of Polymer Science and Engineering, Sichuan University, Chengdu, 610065, China.

出版信息

Mater Today Bio. 2025 Aug 23;34:102238. doi: 10.1016/j.mtbio.2025.102238. eCollection 2025 Oct.


DOI:10.1016/j.mtbio.2025.102238
PMID:40893351
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12398862/
Abstract

Ischemic cardiomyopathy receives significant attention due to its high mortality and morbidity worldwide. Numerous research has revealed that blood supply, ROS, inflammation, and thrombus play pivotal roles in the progression of myocardial damage and remodeling. The central approach for managing ischemic cardiomyopathy is the administration of therapeutic drugs against the pathological mechanism. Despite the development of abundant agents with therapeutic benefits, current therapeutic efficiency is insufficient for further clinical application due to its intrinsic limitations, including poor delivery efficiency and low retention capability. It is urged to seek alternative strategies to improve drug bioavailability and therapeutic index with high biocompatibility. With the emergence of nanotechnology, nanomedicine offer significant improvements to effectively deliver therapeutic molecules for treating ischemic cardiomyopathy. Recently, many biomaterials have been developed to enhance the efficiency of therapeutic drugs for the treatment of myocardial ischemic-related disease. This review summarizes the recent advances of nanomedicine in the treatment of ischemic cardiomyopathy, focusing on antithrombotic therapy, ROS-scavenging therapy, anti-inflammatory therapy, revascularization, and improving electrical conduction. We also discuss the potential limitations and further development of these therapeutic approaches to treat ischemic cardiomyopathy.

摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6842/12398862/3033b83282d2/gr9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6842/12398862/4b5ee2c225c8/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6842/12398862/d3b12bb0ab4c/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6842/12398862/5b0363775635/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6842/12398862/83fec7842bb5/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6842/12398862/bb73c389a2cc/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6842/12398862/5a82116c5cd8/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6842/12398862/061bb860ee77/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6842/12398862/3755d1406706/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6842/12398862/dda9d6115819/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6842/12398862/3033b83282d2/gr9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6842/12398862/4b5ee2c225c8/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6842/12398862/d3b12bb0ab4c/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6842/12398862/5b0363775635/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6842/12398862/83fec7842bb5/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6842/12398862/bb73c389a2cc/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6842/12398862/5a82116c5cd8/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6842/12398862/061bb860ee77/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6842/12398862/3755d1406706/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6842/12398862/dda9d6115819/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6842/12398862/3033b83282d2/gr9.jpg

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本文引用的文献

[1]
Mitochondrial homeostasis restoring peptide-drug conjugates with ROS-responsive NO releasing ability for targeted therapy of myocardial infarction.

J Nanobiotechnology. 2025-7-8

[2]
Reducing the availability of endogenous copper and glucose for cascade starvation therapy and chemodynamic therapy.

Mater Today Bio. 2025-3-24

[3]
Ultrasmall PtIr Bimetallic Nanozyme Treats Myocardial Infarction via Ischemic/Inflammatory Cardiac Microenvironment Remodeling.

ACS Nano. 2025-4-15

[4]
SLC31A1 loss depletes mitochondrial copper and promotes cardiac fibrosis.

Eur Heart J. 2025-3-6

[5]
An injectable and adaptable system for the sustained release of hydrogen sulfide for targeted diabetic wound therapy by improving the microenvironment of inflammation regulation and angiogenesis.

Acta Biomater. 2025-4

[6]
Myocardia-Injected Synergistically Anti-Apoptotic and Anti-Inflammatory Poly(amino acid) Hydrogel Relieves Ischemia-Reperfusion Injury.

Adv Mater. 2025-3

[7]
A Nattokinase-Loaded Nanozyme for Alleviating Acute Myocardial Infarction via Thrombolysis and Antioxidation.

Adv Healthc Mater. 2025-3

[8]
Rational Design of Genetically Engineered Mitochondrial-Targeting Nanozymes for Alleviating Myocardial Ischemic-Reperfusion Injury.

Nano Lett. 2025-1-15

[9]
Peroxynitrite-Free Nitric Oxide-Embedded Nanoparticles Maintain Nitric Oxide Homeostasis for Effective Revascularization of Myocardial Infarcts.

ACS Nano. 2024-11-26

[10]
Engineered Macrophage Membrane-Coated S100A9-siRNA for Ameliorating Myocardial Ischemia-Reperfusion Injury.

Adv Sci (Weinh). 2024-11

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