Background: Rituximab has been widely proposed to treat systemic sclerosis (SSc) by depletion of pathogenic B cells. Nonetheless, the clinical benefit of Rituximab in SSc remains contentious.Objective: This meta-analysis was conducted to systematically evaluate the safety and efficacy profile of Rituximab in SSc patients.Methods: We performed a systematic online query in PubMed, Cochrane, and Web of science.Available studies about the assessment of Rituximab in SSc patients were comprehensively reviewed and investigated.Results: In total, 14 studies comprising 597 participants were enrolled in our analysis. Pooled results showed the durable improvement of mRSS for skin involvement (∆mRSS: 7.00 at 6-month, 9.70 at 12month, and 10.93 at 24-month), while FVC (∆FVC: -0.69 at 6-month, -2.62 at 12-month, -0.67 at 24month) and DLCO (∆DLCO -2.39 at 6-month, -3.28 at 12-month, -0.79 at 24-month) for lung involvement remain stable in SSc patients after Rituximab treatment. And safety profile of Rituximabrelated adverse events rate was 12% in the pooled result. Conclusion:The pooled results of this meta-analysis indicated that Rituximab was well-tolerated, and it was able to generate improvement of cutaneous function and stabilization of pulmonary function in SSc patients.

NAC treatment attenuates skin fibrosis in a BLM-induced mouse model of scleroderma, and this is associated with diminished oxidative stress. The results suggest that NAC may be a potential therapeutic agent for patients with scleroderma.

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Systemic sclerosis is a rare chronic autoimmune disease, which mainly manifests as immune disorders, vascular damage, and progressive fibrosis. The etiology of SSc is complex and involves multiple factors. Both genetic and environmental factors are involved in its pathogenesis. As one of the molecular mechanisms of environmental factors, epigenetic regulation plays an important role in the occurrence and development of systemic sclerosis, which involves DNA methylation, histone modification and non-coding RNA regulation. This review summarizes research advances in epigenetics, including exosomes, lncRNA, and mentions possible biomarkers and therapeutic targets among them.

BackgroundPyroptosis and prostate cancer (PCa) are closely related. The role of pyroptosis-related long non-coding RNAs (lncRNAs) (PRLs) in PCa remains elusive. This study aimed to explore the relationship between PRL and PCa prognosis.MethodsGene expression and clinical signatures were obtained from The Cancer Genome Atlas and Gene Expression Omnibus databases. A PRL risk prediction model was established by survival random forest analysis and least absolute shrinkage and selection operator regression. Functional enrichment, immune status, immune checkpoints, genetic mutations, and drug susceptibility analyses related to risk scores were performed by the single-sample gene set enrichment analysis, gene set variation analysis, and copy number variation analysis. PRL expression was verified in PCa cells. Cell Counting Kit-8, 5-ethynyl-2′-deoxyuridine, wound healing, transwell, and Western blotting assay were used to detect the proliferation, migration, invasion, and pyroptosis of PCa cells, respectively.ResultsPrognostic features based on six PRL (AC129507.1, AC005253.1, AC127502.2, AC068580.3, LIMD1-AS1, and LINC01852) were constructed, and patients in the high-score group had a worse prognosis than those in the low-score group. This feature was determined to be independent by Cox regression analysis, and the area under the curve of the 1-, 3-, and 5-year receiver operating characteristic curves in the testing cohort was 1, 0.93, and 0.92, respectively. Moreover, the external cohort validation confirmed the robustness of the PRL risk prediction model. There was a clear distinction between the immune status of the two groups. The expression of multiple immune checkpoints was also reduced in the high-score group. Gene mutation proportion in the high-score group increased, and the sensitivity to drugs increased significantly. Six PRLs were upregulated in PCa cells. Silencing of AC005253.1 inhibited cell proliferation, migration, and invasion in DU145 and PC-3 cells. Moreover, silencing of AC005253.1 promoted pyroptosis and inflammasome AIM2 expression.ConclusionsOverall, we constructed a prognostic model of PCa with six PRLs and identified their expression in PCa cells. The experimental verification showed that AC005253.1 could affect the proliferation, migration, and invasion abilities of PCa cells. Meanwhile, AC005253.1 may play an important role in PCa by affecting pyroptosis through the AIM2 inflammasome. This result requires further research for verification.