Metabolic syndrome (MetS) is a group of physiological abnormalities characterized by obesity, insulin resistance (IR), and hypertriglyceridemia, which carry the risk of developing cardiovascular disease (CVD) and type 2 diabetes (T2D). Immune and metabolic alterations have been observed in MetS and are associated with autoimmune development. Systemic lupus erythematosus (SLE) is an autoimmune disease caused by a complex interaction of environmental, hormonal, and genetic factors and hyperactivation of immune cells. Patients with SLE have a high prevalence of MetS, in which elevated CVD is observed. Among the efforts of multidisciplinary healthcare teams to make an early diagnosis, a wide variety of factors have been considered and associated with the generation of biomarkers. This review aimed to elucidate some primary biomarkers and propose a set of assessments to improve the projection of the diagnosis and evolution of patients. These biomarkers include metabolic profiles, cytokines, cardiovascular tests, and microRNAs (miRs), which have been observed to be dysregulated in these patients and associated with outcomes.

Chronic migraines have been described chiefly only from a clinical perspective. However, searching for reliable molecular markers has allowed for the discovery of the expression of different genes mainly associated with inflammation, neuro-vascularization, and pain-related pathways. The interest in microRNAs (miRs) that can regulate the expression of these genes has gained significant relevance since multiple miRs could play a key role in regulating these events. In this study, miRs were searched in samples from patients with chronic migraine, and the inclusion criteria were carefully reviewed. Different bioinformatic tools, such as miRbase, targetscan, miRPath, tissue atlas, and miR2Disease, were used to analyze the samples. Our findings revealed that some of the miRs were expressed more (miR-197, miR-101, miR-92a, miR-375, and miR-146b) and less (miR-133a/b, miR-134, miR-195, and miR-340) than others. We concluded that, during chronic migraine, common pathways, such as inflammation, vascularization, neurodevelopment, nociceptive pain, and pharmacological resistance, were associated with this disease.

Objective: To evaluate the predictive risk factors associated with the prevalence of metabolic syndrome (MetS) in adolescents from the western region of Mexico. Materials and Methods: An analytical cross-sectional study was conducted with a sample of 516 adolescents. Anthropometric data, blood pressure, and biochemical determinations were obtained. The diagnosis of MetS was based on the criteria proposed by de Ferranti in 2004. The triglyceride–glucose index (TyG index) was calculated, where a value >4.68 indicates insulin resistance (IR). Risk factors associated with MetS were evaluated using a logistic regression model. The statistical analysis was performed with the level of statistical significance established was p < 0.05. Results: The MetS prevalence was 17.2% among adolescents. One out of every two adolescents with obesity presented with MetS. Abdominal obesity and dyslipidemia are the most common components. Predictors of MetS included male sex, early adolescence, waist-to-height ratio (WHtR) > 0.5, increased body fat percentage, and TyG Index > 4.68 (IR). In the sex-specific analysis, a WHtR > 0.5 and IR were associated with MetS in female adolescents. In male adolescents, IR and body fat percentage were associated with MetS. The WHtR was associated with IR, and hypertriglyceridemia was associated with elevated alanine aminotransferase. Conclusions: In this study, two out of ten adolescents presented with MetS. In boys, a high prevalence of abdominal obesity, hypoalphalipoproteinemia, insulin resistance and MetS was observed. The risk of developing MetS is greater in preadolescent boys with abdominal obesity, high levels of body fat, and a TyG index > 4.68.

Background: Migraine is a disabling neurological disorder where the release of neuropeptides and a local and systemic proinflammatory state prevail. MicroRNAs (miRs) are epigenetic regulators that control the expression of genes involved in inflammation, neovascularization, and pain-related processes. Cytokines mediate the inflammatory state, while miRs can modulate their expression. Methods: This is an analytical and observational study in which subjects with a diagnosis of chronic and episodic migraine and healthy controls were recruited, and the migraine patients were classified by episodic or chronic migraine, as well as with or without aura. Cytokines were measured using the ELISA technique, and the microRNAs hsa-miR-197-3p, hsa-miR-101-3p, and hsa-miR-143-3p were evaluated using qPCR methodology. We also utilized bioinformatic tools, such as miRBase, TargetScan, miRNet, and miRPath, to analyze the interactions and pathways involved. Results: Our findings revealed that hsa-miR-197-3p is elevated in patients without aura (29.91 ± 11.14 with aura vs. 81.10 ± 53.85 without aura, RU; p = 0.021), whereas hsa-miR-143-3p is elevated in episodic migraine (0.0639 ± 0.0227 in EM vs. 0.0308 ± 0.0174, RU p = 0.011). Furthermore, we found higher levels of IL-17 (9.46 ± 1.06 in CM vs. 7.61 ± 2.12 in EM, p = 0.030), IL-6 (4.95 ± 2.84 in CM vs. 1.52 ± 0.98 non-migraine subjects, p = 0.016), and TNFα in chronic migraine patients (0.46 ± 0.24 in CM vs. 0.20 ± 0.05 in non-migraine, p = 0.011 and vs. 0.20 ± 0.13 in EM, p = 0.016). Conclusions: Inflammation is present in migraine regardless of the clinical characteristics of the patients, although it may be accentuated in chronic migraine. Our preliminary findings suggest a potential role for peripheral inflammatory markers, including specific microRNAs (miR-197, miR-101, and miR-143) and cytokines (TNF-α, IL-6, and IL-17A), in the pathophysiology of migraine. These results, although limited by sample size and cross-sectional design, highlight molecular pathways that warrant further investigation.

Rheumatoid arthritis (RA) arises from interactions among immune, stromal, and osteoimmune compartments, supporting interest in agents with multilevel activity, such as celastrol. This narrative review critically integrates evidence on its chemical–pharmacological basis, immunomodulatory mechanisms, cellular effects, and translational potential in RA. Preclinical data show inhibition of inflammatory programs in macrophages and neutrophils, modulation of T- and B-cell responses, suppression of pathogenic fibroblast-like synoviocyte (FLS) functions, and reduced osteoclastogenesis and structural damage. COMM domain-containing proteins 3 and 8 (COMMD3/8) provide the strongest causal validation, while insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3) has biophysical and functional support; numerous inflammatory and metabolic nodes primarily represent downstream signaling. Multicellular models support functional convergence, but intercellular causation in RA remains limited; directional functional evidence for dendritic cell–T-cell modulation comes from non-rheumatoid models, and no persistent synovial reprogramming has been demonstrated. Low bioavailability, multitarget covalent pharmacology, a narrow therapeutic window, and contributions from delivery carriers constrain translational interpretation. Addressing these translational challenges explicitly can help guide future research to improve celastrol’s safety and efficacy, which is essential for clinical application.