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Vascular aging, characterized by structural and functional alterations of the vascular wall, is a hallmark of aging and is tightly related to the development of cardiovascular mortality and age-associated vascular pathologies. Over the last years, extensive and ongoing research has highlighted several sophisticated molecular mechanisms that are involved in the pathophysiology of vascular aging. A more thorough understanding of these mechanisms could help to provide a new insight into the complex biology of this non-reversible vascular process and direct future interventions to improve longevity. In this review, we discuss the role of the most important molecular pathways involved in vascular ageing including oxidative stress, vascular inflammation, extracellular matrix metalloproteinases activity, epigenetic regulation, telomere shortening, senescence and autophagy.

Non-alcoholic fatty liver disease (NAFLD) is an acquired metabolic disease of the liver caused by accumulation of triglycerides in the hepatocytes followed by necrobiotic inflammatory reaction, fibrosis, and even cirrhosis. The accumulation of fatty acids in consequence of insulin resistance lies in the background of the process; the next step of pathogenesis is activation of microsomal polysubstrate systems and the oxidative stress caused by the released free radicals. Obesity, insulin resistance, diabetes mellitus and hyperlipidaemia are important pathogenetic factors. Patients with cholelithiasis and with a history of diabetes mellitus are known to have complications of cholelithiasis more frequently in comparison to those without diabetes. Objective: The aim of the study was the observation of the incidence of cholelithiasis and its complications in patients with NAFLD, as well as the comparison of the incidence of cholelithiasis between healthy persons and patients with NAFLD. Method: Abdominal ultra...

The liver steatosis is a frequent human disease. The most frequent cause of the process is the alcohol consumption. But it also may arise without significant alcohol abuse. This pathogenetic process is called non-alcoholic steatohepatitis (NASH), that is characterized by the same conditions like the alcoholic steatohepatitis. In the pathogenesis of the NASH various factors participate i.e. obesity, diabetes mellitus type II, hyperlipidaemia, pregnancy, variable chemotoxins, parenteral nutrition, jejunoileal bypass, chronic inflammatory diseases, protein deficient nutrition and inborn metabolic diseases. Pathobiochemically the process consists of oxidative stress and lipid peroxidation. This condition comes from the progressive accumulation of the free fatty acids in mitochondria and from the induction of cytochrome P450, CYP 2E1 isoform in hepatocytes and Kupffer cells. The free fatty acids and ketons can cause the induction of CYP 2E1 system, that is why diabetes mellitus and obesity are the two most important factors in the NASH pathogenesis. This article is concerned mainly in the explanation of NASH pathomechanism.