Boron-containing compounds (BCC), particularly boronic acids and derivatives, are being increasingly tested as diagnostic and therapeutic agents. Some effects of BCC involve phenomena linked to the action of steroid or thyroid hormones; among these, are the effects on muscle mass or basal metabolism. Additionally, some toxicology reports on mammals, including humans, sound an alert concerning damage to several systems, among which are the negative effects on the induction of male infertility. Systemic and local mechanisms to explain changes in metabolism and impaired fertility were collected and presented. Then, we presented the putative pharmacodynamic and pharmacokinetic mechanisms involved and demonstrated in these events. In addition, it is proposed that there are adducts of some oxygenated BCC with cis-diols in fructose, an essential source of energy for sperm–cell motility, an uncoupling of sex hormone-binding globulin (SHBG) and its ligands, and the modulation of the DNA synthetic rate. These effects share the reactivity of boron-containing compounds on the cis-diols of key molecules. Moreover, data reporting no DNA damage after BCC administration are included. Further studies are required to support the clear role of BCC through these events to disrupt metabolism or fertility in mammals. If such phenomena are confirmed and elucidated, an advance could be useful to design strategies for avoiding BCC toxicity after BCC administration, and possibly for designing metabolism regulators and contraceptive drugs, among other purposes. Boronic derivatives and carboranes have been proposed and studied in this field.

Peripheral arterial disease (PAD) is a complex, multifactorial atherosclerotic disease that primarily affects the arteries supplying the lower extremities, causing significant occlusion and reduced blood flow. Several studies have found an association between PAD and both genetic and environmental factors, which play a key role in the disease’s pathophysiology. Therefore, in this review, we describe the main genetic variants associated with plaque initiation, progression, and rupture in PAD. Furthermore, we identify different KEGG pathways involved in the pathological processes of these genes. We also describe gene expressions or transcriptomic studies, particularly in biopsies from patients with PAD. These findings could help identify the functional impact of genetic variants on the disease phenotype and, consequently, allow for the development of appropriate interventions that improve patient prognoses.