Endoplasmic Reticulum Stress, NRF2 Signaling and Cardiovascular Diseases in a Nutshell

Insults interfering with endoplasmic reticulum (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.

Authors investigate the role of the inflammatory and oxidative impairment as possible UPR and ER apoptosis inductors in triggering the ER stress response.

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.

Authors summarize evidence that oxidative stress, inflammation and ER stress are closely entwined phenomena. They are involved in the pathogenesis of different settings of cardiovascular diseases.

Authors` own experiences and current literature data are collected, focusing on three precise topics: atherosclerotic plaque, coronary artery disease and diabetes.

The current field of research will provide a platform for study and application to several other conditions in which oxidative stress, ER stress and inflammation are key features.

Future studies in this area may identify the most promising molecules to be investigated as common targets for cardiovascular diseases.