The use of Xenopus oocytes in electrophysiological and biophysical research constitutes a long and successful story, providing major advances to the knowledge of the function and modulation of membrane proteins, mostly receptors, ion channels, and transporters. Earlier reports showed that these cells are capable of correctly expressing heterologous proteins after injecting the corresponding mRNA or cDNA. More recently, the Xenopus oocyte has become an outstanding host–cell model to carry out detailed studies on the function of fully-processed foreign membrane proteins after their microtransplantation to the oocyte. This review focused on the latter overall process of transplanting foreign membrane proteins to the oocyte after injecting plasma membranes or purified and reconstituted proteins. This experimental approach allows for the study of both the function of mature proteins, with their native stoichiometry and post-translational modifications, and their putative modulation by surrounding lipids, mostly when the protein is purified and reconstituted in lipid matrices of defined composition. Remarkably, this methodology enables functional microtransplantation to the oocyte of membrane receptors, ion channels, and transporters from different sources including human post-mortem tissue banks. Despite the large progress achieved over the last decades on the structure, function, and modulation of neuroreceptors and ion channels in healthy and pathological tissues, many unanswered questions remain and, most likely, Xenopus oocytes will continue to help provide valuable responses.

Rheumatoid arthritis (RA) is an autoimmune disease that causes inflammation, pain, and ultimately, bone erosion of the joints. The causes of this disease are multifactorial, including genetic factors, such as the presence of the human leukocyte antigen (HLA)-DRB1*04 variant, alterations in the microbiota, or immune factors including increased cytotoxic T lymphocytes (CTLs), neutrophils, or elevated M1 macrophages which, taken together, produce high levels of pro-inflammatory cytokines. In this review, we focused on the function exerted by osteoclasts on osteoblasts and other osteoclasts by means of the release of exosomal microRNAs (miRNAs). Based on a thorough revision, we classified these molecules into three categories according to their function: osteoclast inhibitors (miR-23a, miR-29b, and miR-214), osteoblast inhibitors (miR-22-3p, miR-26a, miR-27a, miR-29a, miR-125b, and miR-146a), and osteoblast enhancers (miR-20a, miR-34a, miR-96, miR-106a, miR-142, miR-199a, miR-324, and miR-486b). Finally, we analyzed potential therapeutic targets of these exosomal miRNAs, such as the use of antagomiRs, blockmiRs, agomiRs and competitive endogenous RNAs (ceRNAs), which are already being tested in murine and ex vivo models of RA. These strategies might have an important role in reestablishing the regulation of osteoclast and osteoblast differentiation making progress in the development of personalized medicine.

Background/Objectives: Rheumatoid arthritis (RA) is a chronic autoimmune disorder marked by persistent synovial inflammation, progressive joint destruction, and systemic complications. Despite significant progress in targeted therapies, major clinical challenges persist, including heterogeneous treatment responses and therapeutic resistance. This review aims to critically evaluate emerging immunomodulatory strategies—focusing on immune checkpoints, microRNAs (miRNAs), and cell-based therapies—as potential diagnostic and therapeutic tools. Methods: This non-systematic literature review involved a comprehensive analysis of recent studies to investigate emerging immunomodulatory strategies in RA. Special attention was given to immune checkpoint pathways—cytotoxic T-lymphocyte antigen 4 (CTLA-4); programmed death-1 (PD-1) and its ligand, PD-L1; and inducible T-cell costimulator (ICOS)—as well as cell-based therapies. Additionally, miRNA-based interventions were examined for their diagnostic and therapeutic potential. Results: Immune checkpoint modulation has demonstrated preclinical efficacy in attenuating inflammatory responses and restoring immune tolerance. Concurrently, miRNAs have emerged as both biomarkers and therapeutic agents, with exosome-based delivery systems enhancing their function. Cell-based therapies have shown robust immunoregulatory effects with acceptable safety profiles. Notably, integrative strategies that combine checkpoint inhibitors, cell-based interventions, and miRNA delivery exhibit synergistic effects and offer a promising avenue for personalised treatment, when guided by molecular and transcriptomic profiling. The majority of these approaches remain at the preclinical or early translational stage. Conclusions: Targeted immunomodulation is poised to transform RA management. The integration of cell therapies, checkpoint inhibition, and miRNA manipulation with omics technologies holds promise for enhancing therapeutic precision and safety. Advancing towards personalised immunotherapy will necessitate a multidisciplinary and patient-centred effort.

Volcanoes, during their explosive and post-explosive phases, as well as through continuous degassing processes, release a range of pollutants hazardous to human health, including toxic gases, fine particulate matter, and heavy metals. These emissions impact over 14% of the global population living in proximity to volcanoes, with effects that can persist for days, decades, or even centuries. Living conditions in these regions often involve chronic exposure to contaminants in the air, water, and soil, significantly increasing the risk of developing neurological disorders. Prolonged exposure to elements such as lead (Pb), mercury (Hg), and cadmium (Cd), among others, results in the accumulation of metals in the brain, which increases oxidative stress and causes neuronal damage and severe neurotoxicity in animals. An examination of metal accumulation in brain cells, particularly astroglia, provides valuable insights into the developmental neurotoxicity of these metals. Moreover, microglia may activate itself to protect from cytotoxicity. In this review, we consider the implications of living near an active volcano for neurotoxicity and the common neurodegenerative diseases. Additionally, we encourage governments to implement public health strategies and mitigation measures to protect vulnerable communities residing near active volcanoes.

Ultraviolet (UV) radiation is a major environmental stressor that disrupts cellular integrity by inducing oxidative stress, impairing mitochondrial function, and altering immune cell activity, ultimately compromising cellular homeostasis. In this context, carotenoids are widely recognized for their antioxidant and immunomodulatory properties, with C₅₀ carotenoids emerging as a promising subgroup with enhanced biological activity compared with classical C₄₀ carotenoids. Among them, bacterioruberin (BR), a red-pigmented C₅₀ carotenoid mainly produced by haloarchaea, has attracted increasing interest due to its strong antioxidant and cytoprotective potential. Accordingly, this study investigated the mechanisms underlying the protective effects of a bacterioruberin-rich carotenoid extract (BRCE) against UV-induced damage in human peripheral blood mononuclear cells (PBMCs). PBMCs were pre-incubated with BRCE prior to UV exposure and intracellular reactive oxygen species (ROS), mitochondrial membrane potential (Δψm), caspase-3 activation, and the expression of B cell lymphoma 2 (Bcl-2) and granzyme A were evaluated using fluorescence-based assays via confocal microscopy and flow cytometry. BRCE attenuated oxidative stress, preserved mitochondrial membrane potential, reduced caspase-3 activation, and modulated Bcl-2 and granzyme A expression, with more pronounced effects observed at low concentrations. Overall, BRCE exerted a coordinated cytoprotective effect through modulation of oxidative stress, mitochondrial integrity, and apoptosis-related signaling pathways. These findings provide novel insight into the cellular effects associated with the bioactivity of bacterioruberin and support the growing interest in C₅₀ carotenoids as promising photoprotective and immunomodulatory compounds.

Environmental contamination by potentially toxic elements (PTEs) poses a persistent threat to wildlife, yet their accumulation and neurotoxic effects in the avian nervous system remain poorly understood. Although birds are widely recognised as valuable bioindicators of environmental pollution, most biomonitoring studies have focused on conventional tissues such as the liver, kidney, blood and feathers rather than on neural tissues, despite the high susceptibility of the nervous system to toxic injury. This review synthesises current knowledge on the bioaccumulation and neurotoxicity of PTEs in the avian nervous system, with emphasis on the brain, retina, optic pathways and spinal cord. Mercury remains the best-characterised avian neurotoxicant, whereas increasing evidence indicates that lead, cadmium and interactions with essential elements also contribute to neural dysfunction through distinct but partially overlapping mechanisms. Taken together, the available evidence indicates that neurotoxicity cannot be interpreted solely based on total elemental concentrations but also depends on chemical speciation, regional and cellular localisation, disruption of neural metal homeostasis and the intrinsic vulnerability of different neural tissues. Despite increasing evidence of PTE accumulation in neural tissues, important knowledge gaps remain regarding tissue-specific susceptibility and the links between neural damage, behavioural impairment and ecological performance. This review highlights the avian nervous system as an underexplored but biologically relevant target of environmental PTE exposure and highlights the need for more integrative approaches combining chemical, histopathological and functional assessments to improve avian biomonitoring and ecological risk assessment.