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Metabolitos bioactivos generados por la disbiosis intestinal y sus implicaciones fisiopatológicas en la enfermedad cardiovascular


 
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Revista Cubana de Medicina

 ISSN 0034-7523 ISSN 1561-302X

RODRIGUEZ PERON, José Miguel    RODRIGUEZ IZQUIERDO, Mario Miguel. Bioactive metabolites generated by intestinal dysbiosis and their pathophysiological implications in cardiovascular disease. []. , 61, 1, e2584.   25--2022. ISSN 0034-7523.

Introduction:

Dysbiosis is known as the alteration of the symbiotic relationship between the intestinal microbiota and the host is involved in the pathogenesis of atherosclerotic cardiovascular disease.

Objective:

To carry out a documentary review on the pathophysiological mechanisms that relate the bioactive metabolites generated by intestinal dysbiosis with the development and progression of atherosclerotic cardiovascular disease.

Methods:

The Google Scholar search engine was used and free access articles were consulted in Pubmed, SciELO, Lilacs, Cumed and Hinari databases from September 2020 to March 2021. The keywords used for this review were “microbiome”, “gut microbiota”, “dysbiosis”, “atherosclerosis”, “cardiovascular disease” and their English equivalents, according to the Health Sciences (DeCS) descriptor. Original articles, review articles, systematic reviews and meta-analyses after 2015 were considered. A total of 73 articles were reviewed.

Findings:

The pathophysiological relationships between intestinal dysbiosis and cardiovascular diseases are complex, since they influence each other through their endogenous toxins (bioactive metabolites), the circulatory system, immune responses and metabolic changes. Future research should focus on elucidating the underlying molecular players and on identifying whether the pathways that interconnect gut dysbiosis with ACE are causal, correlational, or consequential.

Conclusions:

The accumulated evidence supports that the dysbiosis of the intestinal microbiota is involved in the synthesis of proatherogenic metabolites which modulate the mechanisms involved in the pathophysiology of ACE.

: intestinal microbiota; dysbiosis; atherosclerosis; cardiovascular disease; metabolic syndrome.

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