Mechanisms linking preterm birth to onset of cardiovascular disease later in adulthood

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.

A Novel Antidiabetic Monomers Combination Alleviates Insulin Resistance Through Bacteria-Cometabolism-Inflammation Responses

“…Results of β-diversity of intestinal microbiota reflected by PCA revealed that specific diet and treatment regimens promoted major alterations in the gut microbiota and gut microbial-host related co-metabolites in mice. Furthermore, HFD significantly changed the structure of the community dynamics resulting in decreased abundance of Akkermansia, which is commonly recognized as a beneficial bacterium that is negatively associated with inflammation in the body (Bavineni et al, 2019). Further, Akkermansia supplementation alleviates obesity, inflammatory response in diabetic patients, insulin resistance, glucose tolerance, and other adverse symptoms.…”

Dysbiosis and Prematurity: Is There a Role for Probiotics?

“…Recently, other available data speculate that neonatal colonization contributes to other short- and long-term sequelae of prematurity, such as respiratory distress and bronchopulmonary dysplasia (BPD), retinopathy of prematurity (ROP) [67], somatic growth in early life, and cardiovascular and other non-communicable chronic diseases later in adulthood [68,69,70].…”

Early Life Oxidative Stress and Long-Lasting Cardiovascular Effects on Offspring Conceived by Assisted Reproductive Technologies: A Review

“…Epigenetic modifications refer to dynamic and heritable changes in gene expression without DNA sequence changes. These are profoundly involved in OS responses [ 99 ] and are regarded as potential mechanisms that influence the developmental origins of CVDs later in adulthood [ 100 ]. Maximal epigenetic reprogramming, characterized as ’dynamic’, ’extremely sensitive’, and ’plastic’, occurs during the early stages of life, coinciding with the time that ART procedures take place [ 101 , 102 ].…”

“…From the maternal point of view, advanced maternal age (AMA) [ 154 , 155 ] and OS-increased ART-associated pregnancy complications (e.g., HDP [ 156 , 157 ], GDM [ 158 ], IUGR [ 159 ], and preterm birth [ 100 ]) are frequently associated with cardiovascular dysfunction in the offspring. For example, AMA/HDP/IUGR have been linked with increased blood pressure and/or altered cardiovascular function in offspring [ 154 , 155 , 156 , 159 ], while GDM/preterm birth have been linked with CVDs in offspring [ 100 , 158 ]. Specifically, in a mouse model, it was reported that AMA affects the phenotype of the offspring in a sex-dependent manner: in young adulthood (four months of age), male (but not female) offspring birthed by aged dams presented reperfusion injury and impaired endothelium-dependent relaxation.…”