Multifaceted role of pleiotropic r7rgs g protein beta 5 complex in drug induced liver toxicity

Abstract

Non-alcoholic fatty liver disease (NAFLD) is considered to be a serious health issue to general public and it is enormously expanding in the population. It is a global issue which directly affects gt1.7 billion people (1). NAFLD is seriously has been considered as the next serious global epidemic with estimated prevalence of nearly 25% globally. It is the primary cause of multiple hepatic and extrahepatic complications that is directly associate to NFALD and increasing the health care burden exponentially (1-3). The occurrence of NAFLD and its related medical need is valuable to human life and initiated investigators of different countries to actively explore novel targets which can be transferred for drug development to treat NAFLD and nonalcoholic steatohepatitis (NASH). It has been predicted that drug market of gt$20 billion - $35 billion will be associated to this clinical issues by 2025 (4). Moreover, the intricate complex mechanism and heterogeneity of NAFLD/NASH clinical condition along with pathobiology has increased the situation towards a considerable challenge (3). NAFLD is primarily started by excessive lipid storage and accumulation in liver because of considerable delivery of free FA that results imbalance of degradation and de novo synthesis of lipids. This in turn triggers major inflammatory response especially chronic one which affects other liver cell types (mostly Kupffer and stellate cells) that lead to NASH. But the major problem associated to it is the lack of knowledge of the pathogenesis that includes complex mechanisms and not well understood. Patients having NASH phenotype are reported to possess increased liver-associated mortality with augmented risk of cardiovascular conditions. newline