Abstract
The rupture of saccular intracranial aneurysms (IA) is the commonest cause of non-traumatic subarachnoid hemorrhage (SAH)—the most serious form of stroke with a high mortality rate. Aneurysm walls are usually characterized by an active inflammatory response, and NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) has been identified as the main transcription factor regulating the induction of inflammation-related genes in IA lesions. This transcription factor has also been related to IA rupture and resulting SAH. We and others have shown that autophagy interacts with inflammation in many diseases, but there is no information of such interplay in IA. Moreover, NF-κB, which is a pivotal factor controlling inflammation, is regulated by autophagy-related proteins, and autophagy is regulated by NF-κB signaling. It was also shown that autophagy mediates the normal functioning of vessels, so its disturbance can be associated with vessel-related disorders. Early brain injury, delayed brain injury, and associated cerebral vasospasm are among the most serious consequences of IA rupture and are associated with impaired function of the autophagy–lysosomal system. Further studies on the role of the interplay between autophagy and NF-κB-mediated inflammation in IA can help to better understand IA pathogenesis and to identify IA patients with an increased SAH risk.
Highlights
One in 25 persons can be at risk of intracranial aneurysm (IA), a cerebrovascular disorder which may lead to devastating subarachnoid hemorrhage (SAH) when ruptures occur [1]
The role of inflammation in IA has been appreciated in several reports, and emerging evidence suggests that this role can be critical in the pathogenesis of IA, its rupture, SAH, and their consequences—EBI, DBI, and cerebral vasospasm
The possible involvement of autophagy in IA pathogenesis requires clarification, as some results suggest a direct involvement of this phenomenon in IA induction and development
Summary
One in 25 persons can be at risk of intracranial aneurysm (IA), a cerebrovascular disorder which may lead to devastating subarachnoid hemorrhage (SAH) when ruptures occur [1]. Half of SAH cases result in death in a few weeks after its occurrence, and less than half of the remaining patients is able to conduct a normal life. Efficient IA prevention and detection can decrease the number of life-threatening cases of IA-related SAH. Autophagy is implicated in the pathogenesis of many serious diseases, including cerebral disorders such as cerebral ischemia and resulting brain injury [4], traumatic brain injury [5], intracerebral hemorrhage [6], and others. Some studies show that IA formation and its rupture can be related to the expression of certain autophagy proteins [7,8]. It is justified to explore the link between IA/SAH, inflammation, and autophagy, as an element of IA/SAH pathogenesis and to assess its potential in the prevention, diagnosis, and therapy of IA/SAH
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