@article{1e87cf5e4d134c7f9df8143c852f2d39,
title = "Matrix metalloproteinase-7 promotes chronic kidney disease progression via the induction of inflammasomes and the suppression of autophagy",
abstract = "Deposition of extracellular matrix (ECM), epithelial-mesenchymal transition (EMT) and inflammation are crucial processes in chronic kidney disease (CKD) progression. The matrix metalloproteinases (MMPs) belong to a major enzyme group of proteinases that are involved in ECM degradation. MMP controls multiple biological processes, such as cell proliferation, EMT and apoptosis. The present study identified the roles of MMP7 in CKD progression. We demonstrated the transcriptional profiles of MMPs in kidney tissues of CKD patients in the Gene Expression Omnibus (GEO) data repository. MMP7 mRNA level was markedly upregulated in kidney tissues of CKD patients. MMP7 overexpression activated the NLRP3 and NLRP6 inflammasomes and increased fibrosis-related proteins in kidney cells. MMP7 inhibited oxidative stress-induced apoptosis and rapamycin-induced autophagy. We found that MMP7 expression in the kidney was increased in various CKD animal models. Knockdown of MMP7 affected renal function and renal fibrosis in a folic acid-induced CKD model. The inhibition of MMP7 decreased fibrosis and NLRP3 and NLRP6 inflammasomes and induced autophagy in kidney tissues. Taken together, these results provide insight into targeting MMP7 as a therapeutic strategy for CKD.",
keywords = "Autophagy, Chronic kidney disease, Inflammasome, Matrix metalloproteinase-7, Renal fibrosis",
author = "Zheng, {Cai Mei} and Lu, {Kuo Cheng} and Chen, {Yi Jie} and Li, {Chia Yi} and Lee, {Yu Hsuan} and Chiu, {Hui Wen}",
note = "Funding Information: This study was supported by the Ministry of Science and Technology, Taiwan (MOST 109-2314-B-038-078-MY3 , MOST 110-2314-B-039-018 , MOST 110-2314-B-038-075-MY3 , MOST 111-2314-B-039-021 and MOST 111-2314-B-038-154 ) and the Taipei Medical University-Shuang Ho Hospital ( 111TMU-SHH-02 ). We thank the National RNAi Core Facility at Academia Sinica in Taiwan for providing shRNA reagents and related services. Experiments and data analysis were performed in part through the use of the Medical Research Core Facilities Center, Office of Research & Development at China Medical University, Taichung, Taiwan. Fig. 7 were created with BioRender.com. Funding Information: This study was supported by the Ministry of Science and Technology, Taiwan (MOST 109-2314-B-038-078-MY3, MOST 110-2314-B-039-018, MOST 110-2314-B-038-075-MY3, MOST 111-2314-B-039-021 and MOST 111-2314-B-038-154) and the Taipei Medical University-Shuang Ho Hospital (111TMU-SHH-02). We thank the National RNAi Core Facility at Academia Sinica in Taiwan for providing shRNA reagents and related services. Experiments and data analysis were performed in part through the use of the Medical Research Core Facilities Center, Office of Research & Development at China Medical University, Taichung, Taiwan. Fig. 7 were created with BioRender.com. Publisher Copyright: {\textcopyright} 2022 The Authors",
year = "2022",
month = oct,
doi = "10.1016/j.biopha.2022.113565",
language = "English",
volume = "154",
journal = "Biomedicine and Pharmacotherapy",
issn = "0753-3322",
publisher = "Elsevier Masson",
}