Department of Medical Ultrasound Affiliated Hospital of Nantong University Medical School of Nantong University Nantong China
Yan Zhang
Department of Ultrasound and Central Laboratory Sichuan Academy of Medical Sciences Sichuan Provincial People's Hospital University of Electronic Science and Technology of China Chengdu Sichuan China
Xiaoyang Chen
Department of Medical Ultrasound Affiliated Hospital of Nantong University Medical School of Nantong University Nantong China
Chunyan Zhu
Department of Ultrasound and Central Laboratory Sichuan Academy of Medical Sciences Sichuan Provincial People's Hospital University of Electronic Science and Technology of China Chengdu Sichuan China
Xiulin Dong
Department of Ultrasound and Central Laboratory Sichuan Academy of Medical Sciences Sichuan Provincial People's Hospital University of Electronic Science and Technology of China Chengdu Sichuan China
Weiwei Chen
Department of Medical Ultrasound Affiliated Hospital of Nantong University Medical School of Nantong University Nantong China
Xuejun Ni
Department of Medical Ultrasound Affiliated Hospital of Nantong University Medical School of Nantong University Nantong China
Kun Zhang
Department of Ultrasound and Central Laboratory Sichuan Academy of Medical Sciences Sichuan Provincial People's Hospital University of Electronic Science and Technology of China Chengdu Sichuan China
Yifei Yin
Department of Medical Ultrasound Affiliated Hospital of Nantong University Medical School of Nantong University Nantong China
Abstract Liver fibrosis is a major risk factor for hepatocellular carcinoma origin, and its progression not only correlates with oxidative stress and inflammation, but also is encouraged by autophagy hold‐up. Therefore, new solutions to effectively attenuate oxidative stress and inflammation and coincidently favor autophagy are highly demanded to reverse liver fibrosis, and even hamper its escalation into hepatocellular carcinoma. Herein, the porous manganese‐substituted Prussian blue (PMPB) analogs are harnessed to activate autophagy, scavenge reactive oxygen species (ROS), and suppress inflammation for liver fibrosis therapy. PMPB can effectively inhibit macrophage activation, facilitate macrophage autophagy, eradicate ROS, and blockade cellular cross‐talk, thus impeding further inflammation progression. Moreover, the favorable spontaneous capture of PMPB by Kupffer cells allows more PMPB accumulation in liver to significantly attenuate liver injury and collagen deposition, thereby inhibiting the progression of liver fibrosis. PMPB‐based nanomedicine shows great potentials in promoting autophagy activation, eliminating ROS, inhibiting inflammation, and protecting hepatocytes from oxidative stress‐arised damages, which eventually attenuate the extent of liver fibrosis, holding great promise in clinical translation for treating liver fibrosis.
