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Coronavirus disease 2019 (COVID‐19), caused by severe acute respiratory syndrome coronavirus‐2 (SARS‐CoV‐2), is a pandemic that is claiming hundreds of thousands of lives around the world. Angiotensin‐converting enzyme‐2 (ACE2) is a key player in COVID‐19 due to its pivotal role in the SARS‐CoV‐2 infection. This enzyme is expressed throughout the body and the studies conducted so far have shown that its expression varies according to several factors, including cell type, sex, age, disease states and probably SARS‐CoV‐2 infection. Single‐nucleotide polymorphisms (SNPs) and epigenetic mechanisms, including DNA methylation, histone post‐translational modifications and microRNAs, impact ACE2 expression and may explain structural variation. The understanding of how genetic variants and epigenetic markers act to control ACE2 expression in health and disease states may contribute to comprehend several aspects of COVID‐19 that are puzzling researchers and clinicians. This review collects and appraises the literature regarding some aspects in the ACE2 biology, the expression patterns of this molecule, SNPs of the ACE2 gene and epigenetic mechanisms that may impact ACE2 expression in the context of COVID‐19.

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Summary In the 2 years since the COVID‐19 pandemic was officially declared, science has made considerable strides in understanding the disease's pathophysiology, pharmacological treatments, immune response, and vaccination, but there is still much room for further advances, especially in comprehending its relationship with obesity. Science has not yet described the mechanisms that explain how obesity is directly associated with a poor prognosis. This paper gathers all published studies over the past 2 years that have described immune response, obesity, and COVID‐19, a historical and chronological record for researchers and the general public alike. In summary, these studies describe how the cytokine/adipokine levels and inflammatory markers, such as the C‐reactive protein, are associated with a higher body mass index in COVID‐19‐positive patients, suggesting that the inflammatory background and immune dysregulation in individuals with obesity may be expressed in the results and that adiposity may influence the immune response. The timeline presented here is a compilation of the results of 2 years of scientific inquiry, describing how the science has progressed, the principal findings, and the challenges ahead regarding SARS‐CoV‐2, COVID‐19, and emerging variants, especially in patients with obesity.

Childhood obesity is a global burden affecting millions of children worldwide. It is well-known that the adiposity profile in children is critical for future occurrence of diseases. As a multifactorial disease, obesity is associated with genetic and environmental factors. Epigenetic mechanisms link the plethora of environmental clues to a given phenotype. DNA methylation is the most studied epigenetic mark and its importance in several diseases was acknowledged. In childhood obesity, specifically, the studies show a consistent association between adiposity and methylation at the gene and genome-wide scales. The relationship between DNA methylation and childhood obesity has been proved strong for some genes and pathways. However, the studies are heterogeneous in their design, methodologies, and results. The aim of this review is to discuss this heterogeneity and point out some aspects that should be considered in future studies to clarify the role of DNA methylation in childhood obesity. K E Y W O R D Sadiposity, body mass, childhood obesity, DNA methylation, epigenetics