| Literature DB >> 30753448 |
Mahesh Bavineni1, Trudy M Wassenaar2,3, Kanishk Agnihotri4, David W Ussery3, Thomas F Lüscher5,6, Jawahar L Mehta4.
Abstract
Cardiovascular disease (CVD) rates in adulthood are high in premature infants; unfortunately, the underlying mechanisms are not well defined. In this review, we discuss potential pathways that could lead to CVD in premature babies. Studies show intense oxidant stress and inflammation at tissue levels in these neonates. Alterations in lipid profile, foetal epigenomics, and gut microbiota in these infants may also underlie the development of CVD. Recently, probiotic bacteria, such as the mucin-degrading bacterium Akkermansia muciniphila have been shown to reduce inflammation and prevent heart disease in animal models. All this information might enable scientists and clinicians to target pathways to act early to curtail the adverse effects of prematurity on the cardiovascular system. This could lead to primary and secondary prevention of CVD and improve survival among preterm neonates later in adult life. Published on behalf of the European Society of Cardiology. All rights reserved.Entities:
Keywords: Cardiovascular disease; Dyslipidaemia; Inflammation; Microbiome; Prematurity; Renin–angiotensin system
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Year: 2019 PMID: 30753448 PMCID: PMC6451766 DOI: 10.1093/eurheartj/ehz025
Source DB: PubMed Journal: Eur Heart J ISSN: 0195-668X Impact factor: 29.983