Hypertension is a global epidemic with nearly half of the world's adult population being defined as having a blood pressure (BP) greater than 130/80 mmHg or taking medication for hypertension [1]. Hypertension is associated with a great number of health problems including kidney disease, heart disease, and stroke, with huge social and economic costs [2]. Human and animal research suggests that hypertension can develop in the earliest stage of life or be programmed prenatally [3,4].

Optimal maternal nutrition plays a crucial role in ensuring a healthy pregnancy and normal fetal development. Either nutrient deficit or excess during gestation predisposes to the appearance of many adult diseases, according to the theory of developmental origins of health and disease (DOHaD) [5]. Fetal epigenetic programming could affect gene expression, organ morphology, and cellular function through epigenetic modifications [6]. On this matter, altered fetal phenotypes may increase the risk of many adult diseases, including hypertension.

Epigenetic processes have the potential to initiate alterations in gene expression by inducing modifications in the structure of chromosomes. Examples are DNA methylation and histone modification [7]. DNA methylation is involved in normal cellular development and differentiation, and aberrant DNA methylation of blood pressure (BP)-associated genes participates in the development of hypertension [8]. Histone modifications occur when the N-terminal tail is subjected to a variety of post-translational modifications, including acetylation, phosphorylation, methylation, biotinylation, and sumoylation [9]. Another epigenetic mechanism is mediated by microRNAs (miRNAs), which can act together with the 3′ untranslated region (3′ UTR) of their target mRNAs to induce mRNA decay and translational repression.

Through shifting therapy from adulthood to the perinatal period, adverse programming processes geared toward disease could be postponed or ceased by so-called reprogramming [10]. Nutritional interventions are based on certain particular nutrients, nutraceuticals, and bioactive compounds that could modify epigenetic marks and gene expression [11]. The integration of the emerging knowledge derived from nutrient-gene interaction is required to outline novel strategies to reprogram hypertension and prevent it from happening.

Herein, our review aims to provide insight into how maternal nutrition impacts offspring hypertension, what the mechanisms linking epigenetic programming to hypertension of developmental origins are, and which nutritional interventions are future therapeutic targets through epigenetic regulation to prevent hypertension. A schematic summarizing the interrelationships between maternal nutrition, epigenetic programming, and the developmental origin of hypertension is illustrated in Figure 1.

We retrieved related literature from all articles indexed in the databases Embase, MEDLINE, and Cochrane Library. In this review, gray literature and non-English articles were excluded. Search keywords were as follows: "blood pressure", "hypertension", "developmental programming", "DOHaD", "mother", "maternal", "pregnancy", "gestation", "offspring", "perinatal", "reprogramming", "epigenetics", "DNA methylation", "histone modification", "microRNA", "nutrients", "amino acid", "fat", "fructose", "protein", and "nutrition". On the basis of appropriate references in eligible papers, additional research papers were then selected and evaluated. The last search was conducted on 31 July 2023.