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dc.contributor.authorZununi Vahed, S
dc.contributor.authorBarzegari, A
dc.contributor.authorZuluaga, M
dc.contributor.authorLetourneur, D
dc.contributor.authorPavon-Djavid, G
dc.date.accessioned2018-08-26T04:55:32Z
dc.date.available2018-08-26T04:55:32Z
dc.date.issued2018
dc.identifier.urihttp://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/38364
dc.description.abstractMyocardial infarction (MI) is the main cause of cardiovascular crises that entails serious concerns in mortality, morbidity, and cost to the society. The main therapeutic goal of modern cardiology is to develop novel approaches to minimize inflammation, myocardial necrosis/apoptosis, and enhance cardiac repair after MI. Though MI can be affected by genetic and environmental factors, the search for targeting lifestyle factors has been of greater interest. One such potential factor is the microbiota, the human intestinal microbial community. Although the fundamental data on the role of microbiome on MI is more limited, the disruption of intestinal flora structure provokes MI and poor prognosis. Since gut microbiota is readily modifiable through a variety of interventions, it can be targeted to modulate the host signaling pathways involved in inflammation and MI pathogenesis. Symbiosis bacteria can reduce ischemia/reperfusion injury and inflammation; moreover, they can regulate lipid metabolism, blood pressure, apoptosis, MI size, and overall cardiac survival. In this review, we provide an overview of the development of MI following the dysbiosis microbiota and give an update on a microbiota-based therapeutic strategy to delay or prevent MI.
dc.language.isoEnglish
dc.relation.ispartofPharmacological research
dc.titleMyocardial infarction and gut microbiota: An incidental connection.
dc.typearticle
dc.citation.volume129
dc.citation.spage308
dc.citation.epage317
dc.citation.indexPubmed
dc.identifier.DOIhttps://doi.org/10.1016/j.phrs.2017.11.008


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