Pyroptosis: A possible link between obesity-related inflammation and inflammatory diseases.

The main manifestation of obesity is persistent low-level inflammation and insulin resistance, which is an important factor inducing or promoting other obesity-related diseases. As a proinflammatory programmed cell death, pyroptosis plays an important role, especially in the activation and regulation of the NLRP3 inflammasome pathway. Pyroptosis is associated with the pathogenesis of many chronic inflammatory diseases and is characterized by the formation of micropores in the plasma membrane and the release of a large number of proinflammatory cytokines. This article mainly introduces the main pathways and key molecules of pyroptosis and focuses on the phenomenon of pyroptosis in obesity. It is suggested that the regulation of pyroptosis-related targets may become a new potential therapy for the prevention and treatment of systemic inflammatory response caused by obesity, and we summarize the potential molecular substances that may be beneficial to obesity-related inflammatory diseases through target pyroptosis.

Age- and gender-related difference of ACE2 expression in rat lung.

Epidemiologic data suggested that there was an obvious predominance of young adult patients with a slight female proneness in severe acute respiratory syndrome (SARS). The angiotensin-converting enzyme 2 (ACE2) was very recently identified as a functional receptor for SARS virus and is therefore a prime target for pathogenesis and pharmacological intervention. Rats of both genders at three distinct ages (young-adult, 3 months; middle-aged, 12 months; old, 24 months) were evaluated to determine the characteristic of ACE2 expression in lung and the effect of aging and gender on its expression. ACE2 was predominantly expressed in alveolar epithelium, bronchiolar epithelium, endothelium and smooth muscle cells of pulmonary vessels with similar content, whereas no obvious signal was detected in the bronchiolar smooth muscle cells. ACE2 expression is dramatically reduced with aging in both genders: young-adult vs. old P < 0.001 (by 78% in male and 67% in female, respectively) and middle-aged vs. old P < 0.001 (by 71% in male rats and 59% in female rats, respectively). The decrease of ACE2 content was relatively slight between young-adult and middle-aged groups (by 25% in male and 18% in female, respectively). Although there was no gender-related difference of ACE2 in young-adult and middle-aged groups, a significantly higher ACE2 content was detected in old female rats than male. In conclusion, the more elevated ACE2 in young adults as compared to aged groups may contribute to the predominance in SARS attacks in this age group.