@article{Gao2023, 
author = {Jinfeng Gao and Wusiman Yakufu and Hongbo Yang and Yanan Song and Qiaozi Wang and Qiyu Li and Haipeng Tan and Jing Chen and Dili Sun and Zhengmin Wang and Jinyan Zhang and Xueyi Weng and Juying Qian and Zhiqing Pang and Qibing Wang and Zheyong Huang and Junbo Ge},
title = {Early initiation of ARBs without blood pressure risk via neutrophil membrane-fused pH-sensitive liposomes to reduce cardiomyocyte apoptosis after acute myocardial infarction},
year = {2023},
journal = {Nano Research},
volume = {16},
number = {7},
pages = {9894-9905},
keywords = {Valsartan, early initiation, cardiomyocyte apoptosis, blood pressure, myocardial infarction},
url = {https://www.sciopen.com/article/10.1007/s12274-023-5846-0},
doi = {10.1007/s12274-023-5846-0},
abstract = {Activation of the local renin–angiotensin system (RAS) promotes cardiomyocyte apoptosis and cardiac remodeling after acute myocardial infarction (AMI). As an anti-RAS drug, the effect of Valsartan in the early stage of acute MI is limited by its low drug concentration in the heart and low dosage. Here, by exploiting the inherent nature of neutrophils migrating to the injured myocardium and the local low-pH microenvironment caused by ischemia and hypoxia after myocardial infarction, we designed nanocarrier (NSLP)-hybridized neutrophil membranes and pH-sensitive liposomes (SLPs) for the delivery of Valsartan (NSLP-Val). These functional nanocarriers could mimic neutrophils and are homed to the injured heart; they were also found to respond to a low-pH microenvironment. In the mouse model of MI, we found that NSLP-Val could target the infarct marginal zone and release Valsartan locally in the low-pH microenvironment without affecting hemodynamic stability. Further, locally released angiotensin receptor inhibitors reduced the infarct size and inflammatory response by inhibiting cardiomyocytes. Ultimately, NSLP-Val improved cardiac function and inhibited cardiac hypertrophy and fibrosis.}
}