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Systemic lupus erythematosus (SLE) is a chronic autoimmune disease of unknown aetiology, with the broad range of antibodies affecting various organs and tissues, leading to rapid disability and even to lethal outcome. Our objective was to make an analysis of the results of relevant global studies about genetic mutations, spectrum of antibodies and cytokines involved in the pathogenesis of SLE. The search was conducted in PubMed and Google Scholar platforms using keywords “systemic lupus erythematosus”, “genetic mutations”, “autoantibodies”, “cytokine production”, “sequencing”, “NGS" and "exome". Several genes were found to be involved in the pathogenesis of SLE, the majority of which were associated with B- and T-cell abnormal activation. The results of different studies revealed an association of active SLE with the increase in specific circulating autoantibodies. Based on the results of the current review, a preliminary list of autoantibodies, genes and cytokines associated with the development of SLE was prepared. Future directions will include the assessment of association of genes, antibodies and cytokines in SLE patients from the local Kazakh population, and the development of genetic-immunologic panel for the early diagnosis of this disease.

Objective: This study aimed to investigate the potential therapeutic efficacy of rutin in the management of psoriasis and elucidate its underlying molecular mechanisms., Methods: A systems biology approach, utilizing network pharmacology, was employed to identify and analyze putative targets of rutin relevant to psoriasis. The impact of rutin on the Psoriasis Area and Severity Index (PASI) scores was assessed in an imiquimod (IMQ)-induced murine psoriasis model. Histopathological alterations in the skin lesions were examined using hematoxylin and eosin (H&E) staining. Expression levels of key inflammatory mediators, including Tnf, Hif1a, Ptgs2, Tlr4, Nfkb1, Mtor, and Il2, were quantified using quantitative real-time polymerase chain reaction (qRT-PCR)., Results: A comprehensive analysis revealed 62 potential targets of rutin in the context of psoriasis, with these targets being part of 72 interconnected signaling pathways. In vivo studies demonstrated a significant reduction in PASI scores in rutin-treated mice compared to those in the control group. Additionally, rutin treatment was associated with marked improvements in skin lesions, characterized by reduced crust formation and epidermal thickness. qRT-PCR analysis indicated that rutin administration downregulated the mRNA expression of Tnf, Hif1a, Ptgs2, Tlr4, Nfkb1, Mtor, and Il2 in the lesional skin., Conclusion: These findings suggest that rutin holds promise as a therapeutic agent for psoriasis, as it effectively ameliorates IMQ-induced psoriasis-like skin inflammation in mice through modulation of multiple signaling pathways and inflammatory mediators., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Introduction: The macrophage migration inhibitory factor (MIF) plays a pivotal role in the development of rheumatoid arthritis (RA). Previous research indicates that MIF can trigger the expression of cytokine profiles associated with Th1, Th2, and Th17 responses in peripheral blood mononuclear cells (PBMC) from both RA patients and control subjects (CS). Despite these, few studies to date precisely elucidate the molecular mechanisms involved. The present study aimed to associate the expression of Th differentiation TF (T-bet, GATA-3, RORγt) with MIF receptors (CD44, CD74, CXCR2, 4, 7) and Th1, Th2, and Th17 cytokines in PBMC from CS and RA patients., Method: PBMC from both groups was cultured for 24 h. The expression of the canonical and non-canonical MIF receptors and the TF was determined by flow cytometry. Additionally, multiplex bead analysis was employed to assess the levels of cytokines in the culture supernatants. The findings revealed that T CD4+ lymphocytes in the CS group exhibited a heightened expression of CD74 (p<0.05), whereas RA patients displayed an elevated expression of CXCR7 (p<0.001). Furthermore, T CD4+ lymphocytes from RA patients exhibited greater expression of GATA3, RORγt, and FOXP3, along with elevated levels of pro-inflammatory cytokines compared to the CS group (p<0.001)., Result: These results indicate that CD74 is more prominently expressed in PBMC from the CS group, whereas CXCR7 is more expressed in PBMC from RA patients., Conclusion: We also noted an increased secretion of Th17 profile cytokines in RA, potentially influenced by the activation of FOXP3 via CD74 and RORγt through CXCR7 using the endocytic pathway., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Tumor metastasis is a complex process that is controlled at the molecular level by numerous cytokines. Primary breast and prostate tumors most commonly metastasize to bone, and the development of increasingly accurate targeted nanocarrier systems has become a research focus for more effective anti-bone metastasis therapy. This review summarizes the molecular mechanisms of bone metastasis and the principles and methods for designing bone-targeted nanocarriers and then provides an in-depth review of bone-targeted nanocarriers for the treatment of bone metastasis in the context of chemotherapy, photothermal therapy, gene therapy, and combination therapy. Furthermore, this review also discusses the treatment of metastatic and primary bone tumors, providing directions for the design of nanodelivery systems and future research., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Systemic Sclerosis (SSc) is a systemic autoimmune disease of unknown etiology with a highly complex pathogenesis that despite extensive investigation is not completely understood. The clinical and pathologic manifestations of the disease result from three distinct processes: 1) Severe and frequently progressive tissue fibrosis causing exaggerated and deleterious accumulation of interstitial collagens and other extracellular matrix molecules in the skin and various internal organs; 2) extensive fibroproliferative vascular lesions affecting small arteries and arterioles causing tissue ischemic alterations; and 3) cellular and humoral immunity abnormalities with the production of numerous autoantibodies, some with very high specificity for SSc. The fibrotic process in SSc is one of the main causes of disability and high mortality of the disease. Owing to its essentially universal presence and the severity of its clinical effects, the mechanisms involved in the development and progression of tissue fibrosis have been extensively investigated, however, despite intensive investigation, the precise molecular mechanisms have not been fully elucidated. Several recent studies have suggested that cellular transdifferentiation resulting in the phenotypic conversion of various cell types into activated myofibroblasts may be one important mechanism. Here, we review the potential role that cellular transdifferentiation may play in the development of severe and often progressive tissue fibrosis in SSc., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

In the past decades, scientists have made outstanding efforts to treat diabetes. However, diabetes treatment is still far from satisfactory due to the complex nature of the disease and the challenges encountered in resolving it. Inflammatory factors are key regulators of the immune system's response to pathological insults, organ neogenesis, rejuvenation of novel cells to replace injured cells and overwhelming disease conditions. Currently, the available treatments for type 1 diabetes include daily insulin injection, pancreatic beta cell or tissue transplantation, and gene therapy. Cell therapy, exploiting differentiation, and reprogramming various types of cells to generate pancreatic insulin-producing cells are novel approaches for the treatment of type 1 diabetes. A better understanding of the inflammatory pathways offers valuable and improved therapeutic options to provide more advanced and better treatments for diabetes. In this review, we investigated different types of inflammatory factors that participate in the pathogenesis of type 1 diabetes, their possible dual impacts on the differentiation, reprogramming, and fusion of other stem cell lines into pancreatic insulin-producing beta cells, and the possibility of applying these factors to improve the treatment of this disease., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background: Renal disease in T2DM could arise independently of hyperglycemia, aka non diabetic kidney disease. Its prevalence ranges from 33% to 72.5% among T2DM patients. Specific molecular signatures that distinguish Diabetic Nephropathy from NDKD (FSGS) in T2DM might provide new targets for CKD management., Methods: Five original GEO microarray DN and FSGS datasets were evaluated (GSE111154, GSE96804, GSE125779, GSE129973 and GSE121233). Each of the three groups (DN, FSGS, and Controls) had equal renal transcriptome data (n=32) included in the analysis to eliminate bias. The DEGs were identified using TAC4.0. Pathway analysis was performed on the discovered genes aligned to official gene symbols using Reactome, followed by functional gene enrichment analysis using Funrich, Enrichr..STRING and Network analyst investigated PPI, followed by Webgestalt's pathway erichment. Finally, using the Targetscan 7.0 and DIANA tools, filtered differential microRNAs downregulated in DN were evaluated for target identification., Result: Between the three groups, DN, FSGS, and Control, a total of 194 DEGs with foldchange, >2 & <-2 and P-value 0.01 were found in the renal transcriptome. In comparison to control, 45 genes were elevated, particularly in DN, whereas 43 were upregulated specifically in FSGS. DN datasets were compared to FSGS in a separate analysis. FABP4, EBF1, ADIRF, and ART4 were shown to be among the substantially up-regulated genes unique to DN in both analyses. The transcriptional regulation of white adipocytes was discovered by pathway analysis., Conclusion: The molecular markers revealed might be employed as specific targets in the aetiology of DN, as well as in T2DM patients' therapeutic care., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)