The incidence of chronic diseases (CDs), including type 2 diabetes, cardiovascular disease, and obesity, has increased over the last few decades. CDs are the leading cause of death and disability worldwide.

At the molecular level, overactivation of the NLRP3 inflammasome, a multi-protein complex consisting of NLRP3, ASC, and caspase-1, has been linked to the development of many CDs. The NLRP3 inflammasome can be activated by high glucose, palmitate, cholesterol crystals, ceramide, C-reactive protein, and islet amyloid polypeptide under damage-associated molecular patterns (DAMPs), resulting in caspase-1 cleavage and production of mature IL-1β. IL-1β-induced chronic inflammation may result in damage to the host and eventually lead to the development of CDs. Specifically, DAMPs induce the overproduction of ROS, leading to thioredoxin (TRX)-interacting protein (TXNIP) to dissociate from TRX and activation of the NLRP3 inflammasome. Accumulating evidence has suggested that ROS-generating mitochondria lead to spontaneous NLRP3 inflammasome activation, exacerbating inflammatory responses through multiple downstream events, such as an impairing insulin signal transduction associated with insulin resistance. Targeting the aberrant activation of the NLRP3 inflammasome induced by ROS under DAMPs represents an emerging therapeutic target for CDs.

The aim of this Special Issue is to collate original research and review articles describing advances in this field.

Potential topics include but are not limited to the following:

• The role of ROS-induced NLRP3 inflammasome activation in the pathophysiological processes of CDs, such as type 2 diabetes and cardiovascular disease
• Molecular mechanism of the NLRP3 inflammasome activation under DAMPs
• Interplay between ROS, NLRP3 inflammasome, and metabolic diseases
• Effect of bioactive compounds and nutrients on pathologies correlated with oxidative stress and NLRP3 inflammasome
• Effect of natural compounds on pathologies related to oxidative stress and NLRP3 inflammasome
• New experimental models for evaluation of oxidative stress and the NLRP3 inflammasome activation