Primary membranous nephropathy is a leading cause of nephrotic syndrome in adults, characterized by immune complex deposition in the glomerular basement membrane. Predicting proteinuria remission is essential for guiding treatment decisions, optimizing immunosuppressive therapy, and improving renal outcomes. Traditional prognostic markers, such as anti-PLA2R antibody status and baseline proteinuria levels, offer valuable insights into disease progression. However, recent research has identified additional biomarkers that may enhance risk stratification and refine individualized treatment strategies. Serum-based markers, such as uric acid and inflammatory indices, may indicate systemic changes that impact disease progression. Urinary biomarkers, including microhematuria, α1-microglobulin, and CXCL13, have been proposed as potential predictors of disease activity and remission likelihood. Furthermore, histopathological features, such as glomerular basement membrane thickness, tubulointerstitial injury, and acute kidney injury, provide structural correlates that may inform prognosis. This review explores both established and emerging prognostic indicators across various biological domains. Understanding these predictors can aid in developing personalized therapeutic strategies, optimizing disease management, and improving patient outcomes in primary membranous nephropathy.

Atopic dermatitis (AD) is a prevalent chronic inflammatory skin disorder driven by epidermal barrier defects and dysregulated Th2 cell responses. While therapies primarily address adaptive immunity, the role of Natural Killer (NK) cells remains underappreciated. This review analyzes NK cell dysfunctions in AD pathogenesis, evaluating their contributions to compromised skin immunity, microbial dysbiosis, and secondary infections. Accumulating evidence reveals a systemic deficiency of mature, cytotoxic CD56^dim and NKp80+ NK cell subsets in peripheral blood, correlating with disease severity. Within the cutaneous microenvironment, Staphylococcus aureus subverts defenses by utilizing leukocidins to lyse mature NK cells, while superantigens drive an aberrant, pro-inflammatory CD57⁻NKG2+ phenotype, exacerbating inflammation. Furthermore, localized exhaustion of functional NK cells and failure to produce interferon-gamma directly explains AD patients’ unique susceptibility to severe viral complications like eczema herpeticum. Importantly, treatments such as dupilumab and gut microbiota transplantations demonstrate that these NK cell aberrations are reversible, shifting immunity toward a normalized regulatory state. In conclusion, the NK cell compartment represents a vital regulatory axis bridging innate and adaptive immunity. Targeting this axis, particularly through IL-15 superagonists, offers a promising therapeutic frontier to suppress type 2 inflammation and restore antimicrobial defenses.

Introduction: Myosin heavy chains (MHCs) are the core group of proteins that builds skeletal and cardiac muscle. Their characteristic is determined depending on MHC isoform, its percentage distribution and cross-sectional area of fibers it builds. These variables along with MHC gene expression undergo changes during adaptive and pathological processes. Purpose: The aim of the article was to review significant studies on MHCs; summarize current knowledge in terms of adaptation, aging and pathological processes; provide interpretation and reach conclusions. Methods: The literature review was conducted with topic-related articles found on platforms such as NCSI, PubMed, Google Scholar, using terms “MHC”, “MYH”, “Muscle adaptation”, “myosin heavy chains” and “skeletal muscle” in the searching process. Current Knowledge: During adaptation to physical activity, changes in MHCs are dependant on the type of activity. Endurance training decreases expression of MYH4 gene and increases expression of MYH7. It results in transformation of MHC II towards MHC I and in stimulation of mitochondrial biogenesis. Resistance training favors MHC IIa and hypertrophy. Aging process is associated with increased expression of MHC I but lifelong exercises help to preserve favorable fiber profile. MHC ratios and gene expressions are also altered in pathological conditions, such as obesity, neoplasms and heart disorders. MHCs play a significant role in fracture healing, and their serum levels may reflect soft tissue injuries. Conclusions: MHC isoform distribution is associated with muscle adaptation and dysfunction. Understanding its regulation offers new perspectives in disease prevention, rehabilitation, and therapeutic strategies for muscle and cardiovascular health.

The conceptualization of Parkinson’s disease (PD) has shifted from a strictly central neurodegenerative disorder to a systemic synucleinopathy that may, in some patients, originate in the enteric nervous system. This review synthesizes recent evidence highlighting the potential role of sulfate-reducing Desulfovibrio (DSV) bacteria as candidate pathobionts in the proposed “gut-first” pathogenic cascade. By colonizing anaerobic niches within the colon and metabolizing dietary sulfur compounds, DSV generate hydrogen sulfide (H₂S), a gaseous metabolite that may compromise intestinal barrier integrity and impair mitochondrial function through the inhibition of cytochrome c oxidase. These processes have been associated with ATP depletion, cytochrome c release, and iron-dependent oxidative stress, creating conditions that may favor α-synuclein misfolding and aggregation within enteroendocrine cells. We further examine evidence supporting the retrograde propagation of α-synuclein pathology from the gut to the brain via the vagus nerve—a hypothesis strengthened by experimental findings and epidemiological observations, including studies reporting reduced PD risk following truncal vagotomy. Although the increased prevalence of DSV in PD patients suggests potential applications in prodromal diagnostics and microbiome-based risk stratification, a definitive causal relationship has yet to be established. We therefore discuss key methodological limitations, including biases associated with 16S rRNA sequencing and the current lack of robust in vivo metabolomic evidence. Finally, we consider whether targeted modulation of the intestinal environment, including DSV-specific bacteriophages and [FeFe]-hydrogenase inhibitors, could emerge as a future strategy for influencing early disease processes.