In the modern diet, excessive fructose intake (>50 g/day) had been driven by the increase, in recent decades, of the consumption of sugar-sweetened beverages. This phenomenon has dramatically increased within the Caribbean and Latin American regions. Epidemiological studies show that chronic high intake of fructose related to sugar-sweetened beverages increases the risk of developing several non-communicable diseases, such as chronic obstructive pulmonary disease and asthma, and may also contribute to the exacerbation of lung diseases, such as COVID-19. Evidence supports several mechanisms—such as dysregulation of the renin–angiotensin system, increased uric acid production, induction of aldose reductase activity, production of advanced glycation end-products, and activation of the mTORC1 pathway—that can be implicated in lung damage. This review addresses how these pathophysiologic and molecular mechanisms may explain the lung damage resulting from high intake of fructose.

Infectious agents such as viruses, bacteria, and parasites can lead to cancer development. Infection with the helminthic parasite Schistosoma haematobium can cause cancer of the urinary bladder in humans, and infection with the parasites Clonorchis sinensis and Opisthorchis viverrini can promote cholangiocarcinoma. These three pathogens have been categorized as “group 1: carcinogenic to humans” by the International Agency for Research on Cancer (IARC). Additionally, the parasite Schistosoma japonicum has been associated with liver and colorectal cancer and classified as “group 2B: possibly carcinogenic to humans”. These parasites express regulatory non-coding RNAs as microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), which modulate genic expression in different biological processes. In this review, we discuss the potential roles of miRNAS and lncRNAs encoded by helminthic parasites that are classified by the IARC as carcinogenic and possibly carcinogenic to humans. The miRNAs of these parasites may be involved in carcinogenesis by modulating the biological functions of the pathogen and the host and by altering microenvironments prone to tumor growth. miRNAs were identified in different host fluids. Additionally, some miRNAs showed direct antitumoral effects. Together, these miRNAs show potential for use in future therapeutic and diagnostic applications. LncRNAs have been less studied in these parasites, and their biological effects in the parasite–host interaction are largely unknown.

By 2030, non-communicable diseases will have accounted for more than three-quarters of deaths worldwide. Cardiovascular diseases (CVDs) have been the leading cause of death worldwide for several years. Acute myocardial infarction (AMI) is a CVD characterized by necrosis of the heart at the myocardial level due to prolonged ischemia caused by the reduction or sudden absence of coronary blood supply. The prevalence of AMI is higher in men at all ages. The incidence of AMI has decreased in industrialized nations; however, it has been on the rise in Latin America (LATAM) due to lifestyle changes. These changes have caused the combined incidence of CVDs and unresolved health concerns in LATAM, such as infections and malnutrition. It is well known that periodontitis, a highly prevalent chronic infectious inflammatory disease, has been associated with systemic diseases, such as diabetes, kidney diseases, and AMI. This review addresses proposed aspects of the correlation between periodontitis and AMI, explains the importance of preventing periodontitis and CVDs, and analyzes the preventative measures being implemented in LATAM, particularly in Mexico.

Anxiety is a fear response that triggers a stress reaction with the purpose of defending against or avoiding danger, which is considered physiological, until it becomes excessive and persistent, affecting daily life activities. Non-coding RNAs have been explored in terms of their relationship with diseases, and several of them, such as miRNAs, have been found to be key factors in the development of diseases. Specifically, the expression of long non-coding RNAs (lncRNAs) has been implicated in the development of anxiety through various mechanisms such as nervous system development, synaptic function, neurotransmitter regulation, and neuroinflammation. However, several recent reviews have explored the roles of lncRNAs in various mental diseases (mainly in schizophrenia), and considering that existing reviews do not cover the interaction between lncRNAs and aspects such as neuroimmunity in anxiety disorder pathophysiology, the aim of this literature review is to summarize the current knowledge about the contributions of lncRNAs to the molecular and cellular mechanisms underlying the pathogenesis of anxiety disorders. Additionally, we explore their potential applications in the diagnosis, as well as possible treatment approaches, of these disorders, challenges, and current limitations.

Cancer is a deadly disease and, globally, represents the second leading cause of death in the world. Although it is a disease where several factors can help its development, virus induced infections have been associated with different types of neoplasms. However, in bacterial infections, their participation is not known for certain. Among the proposed approaches to oncogenesis risks in different infections are microRNAs (miRNAs). These are small molecules composed of RNA with a length of 22 nucleotides capable of regulating gene expression by directing protein complexes that suppress the untranslated region of mRNA. These miRNAs and other recently described, such as small RNAs (sRNAs), are deregulated in the development of cancer, becoming promising biomarkers. Thus, resulting in a study possibility, searching for new tools with diagnostic and therapeutic approaches to multiple oncological diseases, as miRNAs and sRNAs are main players of gene expression and host–infectious agent interaction. Moreover, sRNAs with limited complementarity are similar to eukaryotic miRNAs in their ability to modulate the activity and stability of multiple mRNAs. Here, we will describe the regulatory RNAs from viruses that have been associated with cancer and how sRNAs in bacteria can be related to this disease.

Background: Obesity is a multifactorial disease with detrimental effects on health and quality of life; unregulated satiety plays a crucial role in food intake and obesity development. Naringenin (NAR) has shown beneficial effects on lipid and carbohydrate metabolism, although its impact on adiposity and satiety remains unclear. This study reports a Western diet (WD)-induced obesity model in rats, wherein 100 mg/kg of NAR was administered as an anti-obesity agent for 8 weeks; oxidative stress, lipid profile, and satiety biomarkers were then studied, as well as in silico interaction between NAR and cholecystokinin (CCK) and ghrelin receptors. Results: NAR supplementation resulted in a significant decrease in retroperitoneal adipose tissue and liver weight, as compared to the untreated WD group (p < 0.05), potentially associated with a decreased feed efficiency. NAR also inhibited the development of dyslipidemia, particularly by reducing serum triglycerides (p < 0.05). NAR supplementation increased CCK serum levels in the basal diet group, an effect that was abolished by the WD (p < 0.05); likewise, no changes were determined on ghrelin (p > 0.05). In silico data shows that NAR is capable of interacting with the CCK and ghrelin receptors, which suggests a potential for it to modulate hunger/satiety signaling by interacting with them. Conclusions: We conclude that NAR has anti-obesogenic effects and may regulate CCK serum levels, although further research is still needed.