The defining characteristic of neural stem cells (NSCs) is their ability to multiply through symmetric divisions and proliferation, and differentiation by asymmetric divisions, thus giving rise to different types of cells of the central nervous system (CNS). A strict temporal space control of the NSC differentiation is necessary, because its alterations are associated with neurological dysfunctions and, in some cases, death. This work reviews the current state of the molecular mechanisms that regulate the transcription in NSCs, organized according to whether the origin of the stimulus that triggers the molecular cascade in the CNS is internal (intrinsic factors) or whether it is the result of the microenvironment that surrounds the CNS (extrinsic factors).

The complex physiology of eukaryotic cells is regulated through numerous mechanisms, including epigenetic changes and posttranslational modifications. The wide-ranging diversity of these mechanisms constitutes a way of dynamic regulation of the functionality of proteins, their activity, and their subcellular localization as well as modulation of the differential expression of genes in response to external and internal stimuli that allow an organism to respond or adapt to accordingly. However, alterations in these mechanisms have been evidenced in several autoimmune diseases, including systemic lupus erythematosus (SLE). The present review aims to provide an approach to the current knowledge of the implications of these mechanisms in SLE pathophysiology.

The aim of this study was to identity in silico the relationships among microRNAs (miRNAs) and genes encoding transcription factors, ubiquitylation, DNA methylation, and histone modifications in systemic lupus erythematosus (SLE). To identify miRNA dysregulation in SLE, we used miR2Disease and PhenomiR for information about miRNAs exhibiting differential regulation in disease and other biological processes, and HMDD for information about experimentally supported human miRNA–disease association data from genetics, epigenetics, circulating miRNAs, and miRNA–target interactions. This information was incorporated into the miRNA analysis. High-throughput sequencing revealed circulating miRNAs associated with kidney damage in patients with SLE. As the main finding of our in silico analysis of miRNAs differentially expressed in SLE and their interactions with disease-susceptibility genes, post-translational modifications, and transcription factors; we highlight 226 miRNAs associated with genes and processes. Moreover, we highlight that alterations of miRNAs such as hsa-miR-30a-5p, hsa-miR-16-5p, hsa-miR-142-5p, and hsa-miR-324-3p are most commonly associated with post-translational modifications. In addition, altered miRNAs that are most frequently associated with susceptibility-related genes are hsa-miR-16-5p, hsa-miR-374a-5p, hsa-miR-34a-5p, hsa-miR-31-5p, and hsa-miR-1-3p.

Background The human dopamine transporter is the main regulator of dopamine tone and an intricate network exists to regulate the expression, conformation, and kinetics of the hDAT. hDAT dysfunction is directly related to Parkinson’s disease. The objective of this work is to evaluate the differential gene expression in the interactome of the Dopamine transporter in the context of Parkinson’s disease. Methods To do this, we evaluated hDAT interaction data in string-db, mint.bio, IntAct, reactome, hprd and BioGRID, subsequently, data was obtained from the differential gene expression of mRNA and miRNAs for this hDAT interactome in the context of PD. Results The analysis of the differential expression changes of genes of the hDAT interactome in tissues of patients with PD compared with tissues of individuals without PD, allowed to identify an expression pattern of 32 components of the hDAT interactome, of which 31 presented a negative change proportion in PD. Conclusions We found a total of 90 miRNAs that could regulate the expression of 27 components of the hDAT interactome, at the same time, 39 components of the hDAT interactome may participate in 40 metabolic pathways. Together, these findings show a systematic effect on the hDAT-mediated dopamine internalization process in patients with Parkinson’s, which would contribute to a greater susceptibility to neuronal oxidative stress in PD patients.

The immune system is a dynamic network that processes information across multiple biological scales, from molecular recognition of antigens to systemic coordination with the neuroimmune axis and microbiota. At the molecular level, pathways such as NF-κB and JAK-STAT regulate gene expression, integrating signals from pathogens and the organism itself while balancing activation through feedback loops. Cellular and tissue-level dynamics are exemplified by germinal centers, where B-cell hypermutation and clonal selection refine the humoral response, and by immunological synapses that regulate T-cell activation and fate. Systemically, the vagus nerve mediates neuroimmune interactions, while the microbiota co-evolves with the immune system, enhancing its plasticity and robustness. These processes embody antifragility, allowing the immune system to strengthen and expand its capabilities with each challenge. By understanding these multiscale processes, novel strategies emerge for precision medicine, including the modulation of the vagus nerve and microbiota, offering personalized approaches to treat infectious, autoimmune, and chronic diseases.

OBJECTIVE: To evaluate the immunosuppressive treatment response to modified Ponticelli regimen (MPR) and oral corticosteroid (OC) plus tacrolimus (TAC) in patients with primary membranous nephropathy (PMN). METHODS: Retrospective cohort analytical study. Adults patients (>18 years old) with diagnosis of refractory PMN (>50% increase in serum creatinine or a level >1.5mg/dl or proteinuria refractory to 6 months of supportive treatment), proved by renal biopsy and immunofluorescence between 2008 and 2016 from the Nephropathy Registry of Colombia (NEFRORED©) were included. Immunosuppressive treatment response was evaluated from baseline to 6 months after the start of therapy. RESULTS: 128 patients with PMN were included, of which 74 (57%) were female. The most frequent syndromic diagnosis was nephrotic syndrome 90 (70%), followed by asymptomatic urinary disorders 31 (25%). Chronic kidney disease manifested concomitantly in 7 (5%) patients. At the end of 6 months, 86 (67%) cases achieved some degree of remission: 23 (18%) complete response (CR) and 63 (49%) cases with partial response (PR), while 42 (33%) cases did not achieved remission. In the TAC+OC group, CR and PR were seen in 14 (20%) and 33 (47%) patients, respectively; and 9 (16%) and 30 (51%) patients in the MPR group, respectively. No statistically significant differences were found when comparing the immunosuppressive treatment response rate with both treatment groups (p > 0.05). CONCLUSIONS: In the PMN, both immunosuppressive treatments (TAC+OC vs MPR) are comparable. We suggest a clinical follow-up of the anti-PLA2R/THSD7A titres at 6/12 months to be correlated with renal function in subsequent studies.