Pyroptosis is a programmed cell death mechanism with a strong inflammatory response. It mainly depends on the inflammasome to activate proteins of the caspase family to cut gasdermin d-n-terminals (gsdmde-n protein) and activate gsdmde proteins. HMGB-1 drives the activated gsdmde protein to translocate to the membrane, forming holes, cell swelling, and cytoplasmic outflow, which eventually leads to cell membrane rupture and cell pyrosis.

Oxidative stress (OS) and pyroptosis are caused by an imbalance between reactive oxygen species (ROS), endogenous antioxidants and inflammation in response to injury, leading to myocardial toxicity, which can then lead ultimately to heart failure. Although the role of oxidative stress and pyroptosis in heart failure has been identified, prevention strategies have been far from successful. Many studies describe drug therapy for heart failure, including CoQ10, natural plant extracts, animal extracts, or chemically synthesized artificial antioxidants. However, the success of animal modeling in various drug efficacy studies does not translate to good results in humans, and, even if it did, large-scale clinical trials are lacking.

This Special Issue aims to summarize the present knowledge of oxidative stress and pyroptosis in heart failure, including molecular mechanisms, prevention and treatment strategies, drug research, and population experiments. Original research and review articles are both welcome.

Potential topics include but are not limited to the following:

• The prevention of oxidative stress and pyroptosis in heart failure
• Subcellular organelle damage in heart dysfunction induced by oxidative stress and pyroptosis
• Dysregulation of protein regulation in heart dysfunction induced by oxidative stress and pyroptosis
• Role of nitric oxide synthase and anti-inflammation in heart failure
• Role of NADPH oxidase in heart dysfunction induced by oxidative stress and pyroptosis