Crosstalk Between Autophagy and Inflammation in Chronic Cerebral Ischaemia

Abstract

Chronic cerebral ischaemia (CCI) is a high-incidence cardiovascular and cerebrovascular disease that is very common in clinical practice. Although many pathogenic mechanisms have been explored, there is still great controversy among neuroscientists regarding the pathogenesis of CCI. Therefore, it is important to elucidate the mechanisms of CCI occurrence and progression for the prevention and treatment of ischaemic cerebrovascular disorders. Autophagy and inflammation play vital roles in CCI, but the relationship between these two processes in this disease remains unknown. Here, we review the progression and discuss the functions, actions and pathways of autophagy and inflammation in CCI, including a comprehensive view of the transition from acute disease to CCI through ischaemic repair mechanisms. This review may provide a reference for future research and treatment of CCI. Graphical Abstract Schematic diagram of the interplay between autophagy and inflammation in CCI. CCI lead to serious, life-threatening complications. This review summarizes two factors in CCI, including autophagy and inflammation, which have been focused for the mechanisms of CCI. In short, the possible points of intersection are shown in the illustration. CCI, Chronic cerebral ischaemia; ER stress, Endoplasmic reticulum stress; ROS, Reactive oxygen species.

Nose-to Brain Delivery of Resveratrol, a Non-Invasive Method for the Treatment of Cerebral Ischemia

“…Paradoxically, reperfusion therapy after a prolong period of ischemia (>3 h) often leads to further cerebral damage. Ischemia and reperfusion activates a cascade of events including excitotoxicity, driven by the excessive activation of N-methyl-D-Aspartate glutamate receptors; oxidative stress, associated with mitochondrial dysfunction and the increase of reactive oxygen species production; the inflammatory response, which can cause damage due to high concentrations of inflammatory mediators; autophagy, a type of cell death induced by organelle damage and extracellular injury stimulation; and the blood-brain barrier (BBB) breakdown process, initiated by the deterioration of thigh junction proteins at the endothelial cells and aggravated by inflammation [5][6][7]. Unfortunately, establishing an effective treatment for stroke has been unfavorable; therefore, it is indispensable to continue the study of compounds that alleviate the damage induced in animal models in future clinical studies.…”