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Construction of a Band‐Aid Like Cardiac Patch for Myocardial Infarction with Controllable H(2)S Release

Excessive or persistent inflammation incites cardiomyocytes necrosis by generating reactive oxygen species in myocardial infarction (MI). Hydrogen sulfide (H(2)S), a gaseous signal molecule, can quickly permeate cells and tissues, growing concerned for its cardioprotective effects. However, short re...

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Detalles Bibliográficos
Autores principales: Li, Weirun, Chen, Peier, Pan, Yuxuan, Lu, Ling, Ning, Xiaodong, Liu, Jiamin, Wei, Jintao, Chen, Minsheng, Zhao, Peng, Ou, Caiwen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9762300/
https://www.ncbi.nlm.nih.gov/pubmed/36285675
http://dx.doi.org/10.1002/advs.202204509
Descripción
Sumario:Excessive or persistent inflammation incites cardiomyocytes necrosis by generating reactive oxygen species in myocardial infarction (MI). Hydrogen sulfide (H(2)S), a gaseous signal molecule, can quickly permeate cells and tissues, growing concerned for its cardioprotective effects. However, short resident time and strong side effects greatly restrict its application. Herein, a complex scaffold (AAB) is first developed to slowly release H(2)S for myocardial protection by integrating alginate modified with 2‐aminopyridine‐5‐thiocarboxamide (H(2)S donor) into albumin electrospun fibers. Next, a band‐aid like patch is constructed based on AAB (center) and nanocomposite scaffold which comprises albumin scaffold and black phosphorus nanosheets (BPNSs). With near‐infrared laser (808 nm), thermal energy generated by BPNSs can locally change the molecular structure of fibrous scaffold, thereby attaching patch to the myocardium. In this study, it is also demonstrated that AAB can enhance regenerative M2 macrophage and attenuate inflammatory polarization of macrophages via reduction in intracellular ROS. Eventually, this engineered cardiac patch can relieve inflammation and promote angiogenesis after MI, and thereby recover heart function, providing a promising therapeutic strategy for MI treatment.