Asthma therapeutic strategy

The TP receptor requires the G/G protein to activate the Src-Ras-ERKl/2 (extracellular signal-regulated kinase 1 and 2) cascade to induce the proliferative response, which in turn promotes the rapid nuclear translocation of activated ERKl/2 (201). Because TP receptor may be activated by many inflammatory mediators (202-204), these findings suggest new therapeutic strategies that alter the ASM hypertrophy or hyperplasia observed in the chronic airflow obstruction and airway inflammation that characterizes asthma, chronic bronchitis, bronchiolitis obliterans, and chronic obstructive pulmonary disease. 

One feature of asthma that appears to be particularly important is the thickening of the basement membrane of the airway epithelium and the deposition of collagen and other matrix products in the airway wall. It has been suggested that these changes constitute the basis for remodeling of the airway, a process that may predispose to airway hyperresponsiveness and to the development of chronic, persistent asthma symptoms. Thus, therapeutic strategies for wheezy infants must address the possibility that for those who will go on to develop asthma, a prolonged delay in anti-inflammatory treatment leads to permanent loss in pulmonary function. 

Chronotherapeutics, the study of pharmacological response as a function of physiological mood, physical activity, biological rhythms etc. has redefined dmg-delivery strategies in the treatment of diabet, ulcers, cardiac attacks, asthma, smoking cessation and other addictive illnesses (Cullander and Guy 1992). Since 1999 Breimer affirmed that the translation of a PD (pharmakodynamic)-dependent delivery pattern into improved therapeutic outcome is a major challenge for dmg-delivery research (Breimer 1999). 

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