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Consequently, this downregulation results in DNA damage and the subsequent production of DNA repair enzymes such as Poly-ADP Ribose Polymerase-1 (PARP-1), which inactivates glyceraldehyde-3-phosphate dehydrogenase (GAPDH), leading to the accumulation of glyceraldehyde-3-phosphate (GAP), Glucose 6-phosphate (G-6-P), and Fructose 6-phosphate (F-6-P)

Furthermore, programmed necrosis can also be influenced by ROS, which promote the formation of a stable association between two serine/threonine kinases, namely RIP1 and RIP3, which mediate the complex formation of programmed necrosis (Figure 1) (22, 24, 46, 47)

Network pharmacology has identified several therapeutic targets for luteolin, demonstrating its effectiveness in treating conditions like osteosarcoma and lung injury