To summarize the molecular mechanisms underlying oxLDL-induced ferroptosis and pyroptosis, emphasizing their interconnected regulatory networks and discussing therapeutic strategies targeting this cell death axis to mitigate residual inflammatory risk in atherosclerosis.
Key Findings:
OxLDL promotes ferroptosis through dysregulated iron metabolism and impaired antioxidant defenses.
Ferroptosis and pyroptosis are interconnected, with byproducts of ferroptosis activating the NLRP3 inflammasome, suggesting potential therapeutic targets.
Therapeutic strategies targeting the cell death axis may help address residual inflammatory risk in atherosclerosis, including specific inhibitors of ferroptosis and pyroptosis.
Interpretation:
Understanding the integrated cell death network involving ferroptosis and pyroptosis may provide insights into therapeutic approaches for atherosclerotic cardiovascular disease.
Limitations:
The review does not provide experimental data but summarizes existing literature, particularly lacking in direct experimental validation of the proposed mechanisms.
Further research is needed to fully elucidate the therapeutic implications of targeting these pathways in clinical settings.
Conclusion:
The review emphasizes the importance of understanding the mechanisms of ferroptosis and pyroptosis in atherosclerosis for potential therapeutic strategies that could significantly impact clinical outcomes.
