Chiara Mozzini
endoplasmic reticulum (ER) stress, oxidative stress and inflammation in cardiovascular diseases. Insults interfering with ER function lead to the accumulation of unfolded and misfolded proteins in the ER. An excess of proteins folding in the ER is known as ER stress. This condition initiates the Unfolded Protein Response (UPR). When the UPR fails to control the level of unfolded and misfolded proteins, ER-initiated apoptotic signalling is induced. Moreover, the role of the protective nuclear erythroid-related factor 2 (Nrf2)/Antioxidant- Related Element (ARE) and the activation of the pro-inflammatory Nuclear Factor-Kappa B (NF-kB) are analysed. Current literature data are presented, focusing on three topics of related pathologies: atherosclerotic plaque, coronary artery disease and diabetes. Moreover, current evidence suggests the likelihood of a link between venous thromboembolism (VTE) and atherosclerosis, although they have been traditionally considered as different pathological identities. The contribution of neutrophils to human atherogenesis has been underestimated, if compared to their contribution established in VTE.
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