作者: Pawan K. Singal , Neelam Khaper , Vince Palace , Dinender Kumar
关键词:
摘要: Our knowledge of the pathophysiology heart failure has advanced far beyond classic concept hemodynamic overload model and associated neurohumoral changes. Current interest lies in understanding fundamentals cellular defects to identify new molecular targets for therapies. Some target sites being explored are inflammatory cytokines, nitric oxide, oxidative stress apoptosis during remodelling processes such as cardiac hypertrophy dilation. The present review provides an overview chemistry/biochemistry free radicals well a discussion some defense mechanisms that have evolved adapted combat these toxic oxygen species. probable role pathogenesis both from animal data patients is also presented.