Ting Ying

Abstract Ferroptosis, an iron-dependent form of oxidative cell death, has emerged as a key driver of osteoarthritis, yet therapeutic strategies remain limited by the inability to safely eliminate iron–chelate complexes after treatment. Their local accumulation can lead to secondary iron release, oxidative stress, and sustained tissue damage. This study presents a hydrogel-based system that enables selective recognition and removal of these complexes through engineered molecular “memory” sites.

1 Introduction Osteoarthritis (OA) is a prevalent degenerative joint disorder.[1] Growing evidence has highlighted the critical involvement of reactive oxygen species (ROS) in the pathophysiology of OA.[2-5] In the OA pathological microevironment, excessive ROS (e.g., •OH, H2O2, O2•−) act as pivotal drivers of disease progression.[6] The excessive accumulation of ROS can directly damage key cellular structures, while disturbing the redox homeostasis within mitochondria, activating critical...

Conflict of Interest The authors declare no conflict of interest. Supporting Information Filename Description adma70081-sup-0001-SuppMat.docx12.9 MB Supporting Information References 1, , , , Science 2000, 289, 284. 2, , Science 2011, 333, 712. 3, , , , , , , , , , , , Nat. Sustainability 2020, 3, 1052. 4, , , , , , , , , , Nat. Nanotechnol. 2018, 13, 345. 5, , , , , , , , , Chem. Soc. Rev. 2020, 49, 1071. 6, , , , Nat. Rev. Mater. 2021, 6, 294. 7, , , , , Nat. Chem. 2015, 7, 166.