Journal
MECHANISMS OF AGEING AND DEVELOPMENT
Volume 195, Issue -, Pages -Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mad.2021.111467
Keywords
Atherosclerosis; Thrombosis; NLRP3 inflammasome; Acute ischaemic stroke; Interleukin-1?
Categories
Funding
- Ministry of Health - Ricerca Corrente - IRCCS MultiMedica
- Universita' degli Studi di Milano (PIANO DI SOSTEGNO ALLA RICERCA 2015-2017 - TRANSITION GRANT LINEA 1A PROGETTO UNIMI PARTENARIATI H2020 (anno 2020)) [PSR20151720PMAGN_01]
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The activation of the NLRP3 inflammasome-IL-1β pathway is crucial in the onset of acute cerebral atherosclerotic vascular disease and subsequent neurodegeneration. Further studies and clinical trials are needed to evaluate the potential dual role of this pathway in stroke prevention and treatment.
The activation of the NLRP3 inflammasome-IL-1? pathway has been clearly shown to be involved in the pathophysiology of cardiovascular diseases, but its role in cerebral atherosclerotic vascular disease has not been fully clarified. Here we provide an overview on the current knowledge about the relevance of the activation of this mechanism in the onset of acute brain atherosclerotic vascular disease and the subsequent tissue damage. Some variants of NLRP3-related genes seem to reduce the susceptibility to acute ischaemic stroke in selected cohorts, although no clear evidence exists either supporting or excluding any role of this pathway in its pathophysiology. Interestingly, robust experimental and clinical data support a major role of the activation of the NLRP3 inflammasome-IL-1? pathway in the post-event inflammatory cascade which leads to neurodegeneration. This evidence highlights a potential dual role of these molecules in brain pre- and post-ischaemic events, supporting the need for further studies, including clinical trials evaluating the modulation of this pathway for stroke prevention and post-stroke treatment.
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