Fig. 8: Proposed mechanistic model delineating the role of PTPMT1 in cysteine deprivation-induced ferroptosis. | Cell Death & Disease

Fig. 8: Proposed mechanistic model delineating the role of PTPMT1 in cysteine deprivation-induced ferroptosis.

From: Pharmacological targeting of the mitochondrial phosphatase PTPMT1 sensitizes hepatocellular carcinoma to ferroptosis

Fig. 8

The pharmacological inhibition of PTPMT1 by alexidine dihydrochloride (AD) augments the susceptibility of HCC to ferroptosis. On one front, AD treatment facilitates the conversion of ferritin-bound Fe3+ to free Fe2+, enriching the labile iron pool (LIP) in the cytoplasm. Concurrently, pharmacological targeting of PTPMT1 not only induces the emergence of both swollen and donut-shaped mitochondria but also amplifies the metabolic transition from succinate (Suc) to fumarate (Fum) within the mitochondrial TCA cycle. Collectively, these alterations heighten the sensitivity of HCC cells to cystine deprivation-induced ferroptosis.

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