Fig. 5
From: Current understanding of osteoarthritis pathogenesis and relevant new approaches

Pathways of pyroptosis, ferroptosis, and autophagy. a Many factors trigger assembly of the NLRP3 inflammasome, followed by activation of caspase-1 or caspase-11/4/5, which cleaves the gasdermin D (GSDMD) protein and pro-IL-1β and pro-IL-18, resulting in the release of IL-1β and IL-18. b During ferroptotic cell death, intracellular Glu is transported to the extracellular space, and extracellular Cys2 is transported into the cell, where it is then transformed into Cys for GSH synthesis. GPX4 reduces ROS accumulation. Excess iron is the basis for ferroptosis execution. Circulating iron binds with transferrin in the form of Fe3+ and then enters the cells by TFR1. Fe3+ is deoxidized to Fe2+ by the iron oxide reductase STEAP3. Ultimately, Fe2+ is released into a labile iron pool in the cytoplasm from the endosome via DMT1. c The canonical formation of autophagosomes involves the following steps: initiation, nucleation, elongation, closure, and recycling