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Abstract: Vascular ageing can be envisioned as the consequence of the accumulation of reactive oxygen species (ROS) associated with generalized endothelial dysfunction. Oxidative stress arises when the balance between production and removal of ROS favours the pro-oxidation arm. Therefore, ROS have been traditionally considered to be only a toxic by-product of aerobic metabolism. However, it has become apparent that ROS might control many different physiological processes, such as stress response, pathogen defence and systemic signalling. This has lead to the hypothesis that a certain level of ROS is needed physiologically, so much so that an overly increased antioxidant potential might be deleterious for health. Recent evidence has strengthened this notion by correlating cellular response with oxidants and the mechanisms that regulate longevity. Here, we overview current literature on this topic and we will try to convince the reader of the importance of balanced oxidative stress for vascular integrity and healthy ageing. [Copyright &y& Elsevier]

Abstract: The ability to survive to an extremely old age is a consequence of complex interactions among genes, environment, lifestyle and luck. In the last two centuries, life expectancy in western countries has doubled, increasing from 40 to 81 years (79 for males and 82 for females). The candidate factors to determine such mortality reduction are reduced exposure to infections and the subsequent reduction in inflammatory responses, and to some extent, improvement in diet and nutrition. Among the people born at the beginning of the previous century, a small portion of individuals (1 in 10,000 born) have reached 100 years, surviving approximately 20 years more than the general population. The successful longevity of these individuals shows a familial component, possibly genetic, as underlined by the centenarian sibling''s increased chance of reaching 100 years of age compared to the general population. Genetic studies on long living individuals have led to the discovery of potential genetic causes of extreme longevity. These discoveries have highlighted the role of lipid metabolism as a potential key player in the ability to survive to extreme old age. Additional studies on the longevity phenotype have confirmed the role of lipids and lipid-associated cell activities in the predisposition to longevity, from lower eukaryotes to humans. The main focus of this review is the appreciation of demographic survival data and changes in recent diet with the above mentioned genetic and phenotypic biomarkers of longevity, in order to elucidate hypotheses on mechanisms of slow aging and disease resistance. [Copyright &y& Elsevier]

The prototype of long pentraxins, Pentraxin 3 (PTX3), is an evolutionarily conserved multifunctional, pattern-recognition protein constituted by a cyclic multimeric structure. PTX3 interacts with a variety of ligands, such as growth factors, extracellular matrix components, molecules of the complement cascade, pathogens recognition proteins, angiogenetic and adhesion molecules. PTX3 could be considered as a molecular link between innate and adaptive immunity as well as between focal and circulating responses during inflammation. In fact, it modulates the functions of resident dendritic cells and circulating lymphocytes. Recent evidence demonstrates that manipulation of PTX3 may produce even opposite effects depending on which target organ is considered and the physiopathological context. In the present review we discuss the good and bad cops of PTX3 concerning multifacted effects on inflammation, innate immunity, brain diseases and tumorigenesis. Finally, a perspective on PTX3 and autophagy is provided as a convergent pathway. [ABSTRACT FROM AUTHOR]