The skin is the largest organ of the human body in contact with the outside world. Different are its functions: body temperature regulation, mechanical barrier, coating, and sensory activity are just to name a few. Like any other part of the human organism, it too undergoes the phenomenon of aging, a complex biological process classified as chronological aging. Although this is a natural and inevitable physiological process, certain external factors have been shown to have an important impact. One of these, much discussed in recent years, is diet. The relevance of diet to the clinical features of skin aging, particularly the biochemical and histological changes that occur in it, is now well established. Lately, there has been a growing focus on which foods can be considered skin‐friendly and which cannot. Açai berries, Moringa oleifera, and spirulina are just some of the emerging nutrients that counteract skin aging because of their potent antioxidant properties. Conversely, foods high in trans‐fatty acids, refined sugars are related to accelerated skin aging as they are associated with the production of advanced glycation end products. Due to the interest generated in recent years on the subject, a subspecialty of anti‐aging medicine called “nutricosmetics” has even emerged. This review aims to highlight the studies emerging in the last five years regarding what can be considered “skin‐friendly” foods in contrast to what can be considered “skin‐unfriendly” habits, taking into consideration studies regarding the innovations recently developed in terms of nutrients and skin aging strategies.

Endocrine-disrupting chemicals (EDCs) are a growing health hazard for humankind and respiratory health in particular. Such chemical compounds are present in the environment and food and may interfere with physiological processes through interference with functions of the endocrine system, making humans more susceptible to various types of diseases. This review aims to discuss the effects of EDCs on the respiratory system. Exposure to EDCs during fetal development and adulthood increases susceptibility to respiratory diseases such as asthma, COPD, and pulmonary fibrosis. EDCs are both multiple and complex in the ways they can act. Indeed, these chemicals may induce oxidative stress, modify cell proliferation and differentiation, interfere with tissue repair, and modulate the inflammatory response. Moreover, EDCs may also break the integrity of the blood–air barrier, allowing noxious substances to penetrate into the lung and thus enhancing the opportunity for infection. In conclusion, the scientific evidence available tends to indicate that EDCs exposure is strongly linked to the initiation of respiratory disease. Further research will be important in discovering the underlying molecular mechanisms and devising preventive and therapeutic measures.

Background/Objectives: Traumatic brain injury (TBI) disrupts both the intestinal epithelium and blood–brain barrier (BBB), contributing to oxidative stress, neuroinflammation, and behavioral impairments. Vitis vinifera leaf (VVL) extract possesses antioxidant and anti-inflammatory properties, but its protective effects on the brain–gut axis following TBI remain unclear. This study aimed to evaluate whether VVL supplementation preserves barrier integrity and improves neurobehavioral outcomes after TBI. Methods: A murine model of TBI was used, with animals receiving daily oral supplementation of the VVL extract. Neurobehavioral performance was assessed through behavioral testing, while histopathological examinations, biochemical assays, and gene expression profiling were performed to evaluate neuronal and intestinal integrity, antioxidant defense, and inflammatory responses. Results: VVL supplementation significantly alleviated anxiety- and depression-like behaviors and preserved the structural integrity of neuronal and intestinal tissues. Antioxidant defense mechanisms were strengthened, as shown by increased catalase and superoxide dismutase activities, together with upregulation of Nrf2 and HO-1 expression. Tight junction proteins, including ZO-1 and occludin, were upregulated in both brain and gut tissues, reflecting improved barrier integrity. Furthermore, VVL markedly reduced pro-inflammatory cytokine expression. Conclusions: VVL extract confers dual protection of the gut and brain barriers after TBI by enhancing endogenous antioxidant defenses, maintaining tight junction integrity, and suppressing inflammation. These findings suggest that VVL may represent a natural therapeutic strategy to mitigate oxidative stress, neuroinflammation, and behavioral dysfunctions associated with TBI.

Fumonisin B1 (FB1), a mycotoxin commonly found in contaminated food and feed, has been increasingly implicated in neurotoxicity, although its mechanisms remain poorly understood. This study investigates the neurotoxic potential of FB1 in human SH‐SY5Y neuroblastoma cells, both undifferentiated and RA‐differentiated, and evaluates the protective effect of bromelain, a natural proteolytic enzyme with antioxidant and anti‐inflammatory properties. Cells were exposed to 50 μM FB1 for 24 h, with or without co‐treatment with bromelain (10 or 50 μg/mL). FB1 significantly reduced cell viability and triggered reactive oxygen species (ROS) production, mitochondrial membrane depolarization, lipid peroxidation, inflammatory cytokine release (IL‐6 and TNF‐α), and apoptosis, particularly in differentiated cells. Bromelain co‐treatment attenuated these effects in a dose‐dependent manner, preserving mitochondrial function, reducing oxidative and inflammatory markers, and lowering apoptotic cell death. These findings emphasize the neurotoxic risk posed by FB1 and highlight bromelain as a promising multi‐target protective agent. Identifying effective countermeasures against environmental neurotoxins is crucial for public health and disease prevention.

Pulmonary arterial hypertension (PAH) is a severe, progressive disease characterized by elevated pulmonary arterial pressure and increased vascular resistance. This hemodynamic strain forces the right ventricle to pump against a high‐pressure system, ultimately leading to right‐sided heart failure and death. The pathogenesis of PAH involves a complex interplay of vasoconstriction, chronic inflammation, and pathological remodeling of the pulmonary vessel walls—specifically hypertrophy of the smooth muscle and intimal layers—driven by molecular imbalances and genetic predispositions. Current FDA‐approved therapies primarily manage symptoms through vasodilation but fail to directly target the underlying vascular remodeling. Imatinib, a tyrosine kinase inhibitor originally developed for oncological indications, has emerged as a potential disease‐modifying agent for PAH. By inhibiting platelet‐derived growth factor receptors (PDGFR), imatinib targets the aberrant proliferation of smooth muscle cells, offering a mechanism to potentially reverse or arrest vascular remodeling. Clinical trials, including the IMPRES study, have demonstrated encouraging hemodynamic improvements in patients with severe PAH refractory to standard therapies. However, systemic safety concerns and dose‐dependent adverse reactions have limited its clinical approval. This review examines the pharmacological rationale for imatinib, its impact on vascular structure, and the safety signals observed in long‐term studies. Furthermore, it discusses emerging strategies, such as inhaled formulations and pharmacogenetic approaches (e.g., the PIPAH study), aimed at enhancing the efficacy‐to‐safety ratio of kinase inhibitors to improve long‐term outcomes for patients with PAH.

This study investigated the immunomodulatory effects of PFOS and glyphosate (GLY), both individually and in combination, on the whole blood of three ruminant species (cow, goats, and sheep) exposed ex vivo to environmentally relevant concentrations. The research focused on key biomarkers of oxidative stress (MDA), inflammation (myeloperoxidase activity, nitrite production), and immune function (TNFα and IL‐6 cytokine production, both at baseline and following LPS stimulation). Results indicated species‐specific differences in oxidative stress response, with sheep and goats showing higher MDA levels under combined PFOS and GLY exposure. Furthermore, co‐exposure exacerbated inflammatory responses (MDA activity and NO2‐ production) in LPS‐stimulated sheep and goats. Critically, a synergistic effect of PFOS and GLY co‐exposure significantly increased both TNFα and IL‐6 production across all species, even without LPS stimulation, suggesting a heightened pro‐inflammatory state. These findings raise concerns about the potential of these contaminants to disrupt immune homeostasis in grazing animals, impacting their health, productivity, and disease resistance, and potentially posing risks to human health through food chain contamination. The study highlights the need for further research to elucidate the underlying molecular mechanisms and assess the long‐term effects of chronic exposure to these contaminants on animal health and potential human health risks.