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Fig. 8 | Molecular Medicine

Fig. 8

From: Increased hemoglobin and heme in MALDI-TOF MS analysis induce ferroptosis and promote degeneration of herniated human nucleus pulposus

Fig. 8

A potential mechanism by which heme iron induces ferroptosis and degeneration of human nucleus pulposus cells. Heme enters the cell through carrier proteins and is degraded by HO-1. This process releases free ferrous ions. Excessive free ferrous iron is oxidized to trivalent iron through the Fenton reaction in the presence of hydrogen peroxide that is metabolized by the cell, forming dangerous hydroxyl free radicals, which lead to lipid peroxidation and ferroptosis (middle). The substrates of peroxidation are polyunsaturated fatty acids (PL-PUFAs), and the GPX4-glutathione axis can eliminate peroxidized PL-PUFA-OOH (left). The MALDI-TOF MS analysis clearly shows the ferroptosis-related metabolic network, which involves sphingolipid metabolism, the tricarboxylic acid (TCA) cycle, arachidonic acid (AA) metabolism, and tryptamine metabolism-related molecules (right)

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