1,721,195 research outputs found
Enhancing the Efficacy of Hepatocellular Carcinoma Chemotherapeutics with Natural Anticancer Agents
No full textRole of oxidative stress in the pathogenesis of cancer
No full textCarcinogenesis is a complex multi-step process
depending on several endogenous and exogenous
factors. A large number of evidences highlights the
important role of oxidative stress in cancer
development and progression. Oxidative stress
occurs as consequence of the cell accumulation of
reactive oxygen species (ROS) or reactive nitrogen
species (RNS). ROS and RNS are generated by
several different insults (i.e. UV light, inflammation,
air pollution, etc.). Physiologically, reactive oxygenmetabolites react with several bio-molecules such as lipids, nucleic acids and
proteins, but when their amount is excessively increased a permanent
structural and/or functional modification of the biological molecules may
occur. This mechanism represents the main way by which the products of
oxidative stress may induce carcinogenesis. On the other hand, since
oxidative stress is caused by an imbalance between the production of reactive
oxygen and cell ability to readily detoxify the reactive intermediates or easily
repair the resulting damage, another strategy to promote cancer is linked to
the less antioxidant capacity of an organism, too.
In this chapter we describe the role of oxidative stress in cancer
development and progression, focusing mainly our attention on the
mechanisms and molecules deregulated during oxidative damage, knowledge
that could be useful for improvement of anticancer gene therapy
Hedgehog/hyaluronic acid interaction network in nonalcoholic fatty liver disease, fibrosis, and hepatocellular carcinoma
No full textHepatitis C Virus and Nonalcoholic Fatty Liver Disease: Similar Risk Factors for Necroinflammation, Fibrosis, and Cirrhosis
No full textn
Toll-like receptor-mediated signaling cascade as a regulator of the inflammation network during alcoholic liver disease
Full text linkChronic abuse of alcohol leads to various histological abnormalities in the liver. These are conditions collectively known as alcoholic liver disease (ALD). Currently, ALD is considered to be one of the major causes of death worldwide. An impaired intestinal barrier with related endotoxemia is among the various pathogenetic factors. This is mainly characterized by circulating levels of lipopolysaccharide (LPS), considered critical for the onset of intra-hepatic inflammation. This in turn promotes hepatocellular damage and fibrosis in ALD. Elevated levels of LPS exert their effects by binding to Toll-like receptors (TLRs) which are expressed by all liver-resident cells. The activation of TLR signaling triggers an overproduction and release of some cytokines, which promote an autocatalytic cascade of other proinflammatory signals. In this review, we provide an overview of the mechanisms that sustain LPS-mediated activation of TLR signaling, reporting current experimental and clinical evidence of its role during inflammation in ALD
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