Molecular basis of chronic inflammation in lung diseases: new therapeutic approach.

摘要: There is increasing evidence that histone acetylation, controlled by acetyltransferases (HAT), reversed deacetylases (HDAC) plays a critical role in the process of regulation inflammatory genes and mediating anti-inflammatory effects corticosteroids asthma patients. an increase HAT activity asthmatics, which leads to increased expression multiple are regulated proinflamatory factors, such as nuclear factor NF-kappaB. Reduction HDAC activity, secondary oxidative nitrative stress severe inflammation, may account for amplified inflammation chronic obstructive pulmonary disease (COPD). Corticosteroids switch off through inhibition recruitment HDAC2 activated transcription complex. Several new strategies control inflammations COPD, aiming at restoration HDAC-2 and/or mitigation HAT-related signaling preclinical clinical development.