Cross-Communication of Cuproptosis and Regulated Cell Death in Human Pathophysiology

Molecular mechanisms of pyroptosis triggered by excess Cu. Excessive Cu influx through CTR1 leads to mitochondrial stress and activation of the caspase-3/GSDMD-dependent pyroptosis signaling pathway. GSDMD, downstream of caspase-3, forms an N-terminal domain that perforates the cell membrane, causing cell swelling, rupture, and release of inflammatory factors and DAMPs. Moreover, GSDMD is the effector protein of caspase-8/ASC/11, which undergoes cysteine cleavage to generate the N-terminal domain and promote pyroptosis. The GSDMD-dependent cell death pathway is mainly triggered by various aberrant signals, including the release of inflammatory factors that initiate a cascade of intracellular inflammatory responses (e.g., NF-κB).

Publication

The Cross-Communication of Cuproptosis and Regulated Cell Death in Human Pathophysiology. (2024) Kuan-Hao Tsui, et al. Int J Biol Sci. 2024;20(1):218-230. Figure: F4. Homo sapiens

Disease mentions