Pycard, also known as PYD and CARD domain containing or ASC (apoptosis-associated speck-like protein containing a caspase activation and recruitment domain), is a pivotal adaptor protein in inflammasome assembly and activation. It contributes to innate immunity and is involved in multiple pathways such as NOD-like receptor signaling pathway. It plays an essential role in the pathogenesis of various diseases including atherosclerosis, restenosis, tendinopathy, COPD, rheumatoid arthritis, and psoriasis [1-3, 6, 10].

In tendinopathy, pristimerin alleviates the disease by promoting the autophagic degradation of AIM2 through a PYCARD/ASC-dependent manner, enhancing the K63-linked ubiquitin chains of PYCARD/ASC at K158/161 [1]. In COPD, PYCARD is a crucial PANoptosis-related gene, positively related to NOD-like receptor signaling pathway and promoting immune cell infiltration [2]. In the context of neointima formation, Pycard deficiency in knockout mice reduces circulating miRNA profile, inhibits Mir17 seed family maturation, and prevents vascular injury-induced neointima formation by promoting chaperone-mediated autophagic degradation of AGO2 in adipose tissue [3].

In conclusion, Pycard is a key gene in inflammasome-related processes and innate immunity. Studies using gene knockout mouse models have revealed its roles in multiple disease areas, including tendinopathy, COPD, and neointima formation. Understanding Pycard's functions provides potential therapeutic targets for these diseases.