Cerebral ischemia reperfusion injury: from public health perspectives to mechanisms

Abstract

Cerebral ischemia/reperfusion injury has emerged as an intricate mechanism. However, identification of wide-ranging mechanisms which mechanistically regulate reperfusion injuries have significantly improved our understanding. Recent advancements in our knowledge about the molecular consequences of ischemia and reperfusion might be advantageous in the development of innovative therapeutic strategies for the treatment of patients with ischemia and reperfusionassociated organ dysfunction and tissue inflammation. Some of the extensively studied mechanisms of reperfusion injury consist of oxidative stress, mitochondrial mechanisms, infiltration of leukocytes, activation/aggregation of the platelets, complement activation, and disruption of the blood-brain-barrier (BBB), which eventually results in the brain oedema or haemorrhagic transformations. In this review, we have attempted to provide a review of the protein networks involved in the regulation of cerebral ischemia reperfusion injury and how different natural products have shown potential in the amelioration of reperfusion induced injuries.

Advances in the application of manganese dioxide and its composites for theranostics

“…124 However, the main obstacle to neuronal survival is reperfusion injury in acute ischemic stroke. 125,126 Li et al 127 employed macrophage-camouflaged honeycomb MnO 2 nanospheres loaded with fingolimod (FTY) to rescue the ischemic penumbra. The MnO 2 nanospheres facilitate the accumulation of cell adhesion molecules that are over-expressed on the damaged vascular endothelial cells at the site of brain damage through recognition mediated by macrophage membrane proteins, thereby enabling T 1 MRI (Fig.…”

Knockdown of FOXO4 protects against OGD/R‑induced cerebral microvascular endothelial cell injury and regulates the AMPK/Nrf2/HO‑1 pathway through transcriptional activation of CTRP6

“…At present, the most effective clinical treatment for cerebral ischemia is to re-establish effective blood supply and restore cerebral perfusion in the ischemic area by mechanical thrombectomy and intravenous thrombolysis with drugs such as anticoagulants and, antiplatelet and thrombolytic drugs ( 3 ). However, inflammation and oxidative stress during reperfusion can cause secondary injury to brain tissue, resulting in brain dysfunction ( 4 ). This pathophysiological process is known as cerebral ischemia/reperfusion injury (CIRI).…”

Sirtuin-3 activates the mitochondrial unfolded protein response and reduces cerebral ischemia/reperfusion injury

“…Cerebral ischemia/reperfusion (I/R) injury results from the restoration of blood flow to the ischemic brain after a stroke, cardiac arrest or traumatic brain injury 1 , 2 . I/R injury is initiated in the ischemic phase, mainly as a result of deficiency in oxygen or nutrients supply to neural cells 3 .…”