The role of the microbiota-gut-brain axis in the pathogenesis of ischaemic stroke

Abstract

Background. Currently, stroke is the second leading cause of mortality and the third leading cause of disability in the world despite advances in treatment and prevention; therefore, it is necessary to identify new pathogenetic targets in the therapy of ischaemic stroke (IS). Recent studies have emphasised the significant contribution of the microbiota-intestinal-cerebral axis to the pathogenesis of IS. Aim - to critically analyse the data on the role of the microbiota-gut-brain axis in the pathogenesis of MI in peer-reviewed sources indexed in the Pubmed and Russian Science Citation Index databases for the period 2019-2024 using the following keywords: "gut microbiota", "ischemic stroke", "pathogenesis".

Conclusion. It has been demonstrated that AI induces intestinal dysbiosis by damaging the intestinal mucosa and the intestinal barrier through the secretion of DAMPs, activation of TLRs and the sympathoadrenal system, inducing intestinal dysbiosis; opportunistic microbiota is able to exert a pathogenic effect on the focus of ischaemic injury through its signalling molecules and metabolites, such as LPS and TMAO, reduced SCFA synthesis increase the synthesis of pro-inflammatory cytokines in the ischaemic zone cause phenotypic polarisation of microglia to M1, thereby supporting neuroinflammation; in addition, opportunistic microbiota triggers the kynurenine metabolic pathway, thereby reducing melatonin synthesis and its neuroprotective effects mediated by increased expression of Bmal1 and potentiation of the Nrf2 pathway.