{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yao P"],"funding":["the Sichuan Science and Technology Program","Health Commission of Sichuan Province Medical Science and Technology Program","the Open Project of Key Laboratory of Nuclear and Radiation Damage Mechanisms and Treatment Technologies at Chengdu Medical College of Sichuan Province, The Second Affiliated Hospital of Chengdu Medical College, Nuclear Industry 416 Hospital"],"pagination":["949-965"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12935853"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["58(3)"],"pubmed_abstract":["The kidney exhibits a remarkable capacity for repair following acute injury; however, unchecked or persistent inflammation often drives maladaptive repair, fibrosis, and progression to chronic kidney disease (CKD). Inflammation is pivotal in this process, characterized by complex, bidirectional cross talk between diverse immune cell populations and resident renal intrinsic cells. This intricate interplay critically dictates the balance between successful regeneration and pathological scarring. This review delves into the fundamental immunologic mechanisms underpinning kidney injury and maladaptive repair, analyzing the specific roles of key immune and intrinsic renal cell types, their complex communication networks, and critical signaling pathways. Recognizing the limitations of convention"],"journal":["International urology and nephrology"],"pubmed_title":["Precision nanotherapeutics for kidney disease: targeting inflammation and maladaptive repair."],"pmcid":["PMC12935853"],"funding_grant_id":["2023JDRC0089","2024ZDSYS09","24WXXT09"],"pubmed_authors":["Zheng Y","Yao P","Li C"],"additional_accession":[]},"is_claimable":false,"name":"Precision nanotherapeutics for kidney disease: targeting inflammation and maladaptive repair.","description":"The kidney exhibits a remarkable capacity for repair following acute injury; however, unchecked or persistent inflammation often drives maladaptive repair, fibrosis, and progression to chronic kidney disease (CKD). Inflammation is pivotal in this process, characterized by complex, bidirectional cross talk between diverse immune cell populations and resident renal intrinsic cells. This intricate interplay critically dictates the balance between successful regeneration and pathological scarring. This review delves into the fundamental immunologic mechanisms underpinning kidney injury and maladaptive repair, analyzing the specific roles of key immune and intrinsic renal cell types, their complex communication networks, and critical signaling pathways. Recognizing the limitations of convention","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Mar","modification":"2026-07-11T03:15:00.901Z","creation":"2026-07-11T03:11:40.727Z"},"accession":"S-EPMC12935853","cross_references":{"pubmed":["40900261"],"doi":["10.1007/s11255-025-04714-9"]}}