Mitochondrial abnormalities are crucial in the progression of systemic lupus erythematosus (SLE), with key elements like mitochondrial DNA mutations, oxidative stress, and immune metabolic reprogramming leading to cellular death. These dysfunctions result in an array of SLE symptoms, pointing toward mitochondrial pathways as potential therapeutic targets for improved patient outcomes.

A bibliometric analysis was performed to identify the current research status and future directions in the field of COVID-19 vaccinations in patients with rheumatic diseases by pooling published research articles and reviews through the Web of Science Core Collection.

Apoptotic cell (AC)-conditioned mesenchymal stem cells exhibited enhanced therapeutic effects in lupus-prone MRL/lpr mice, partially mediated by cyclooxygenase 2/prostaglandin E2. Precondition ACs may be a new strategy for mesenchymal stem cell transplantation in treating systemic lupus erythematosus.

Microarray datasets of rheumatoid arthritis (RA), osteoarthritis, and healthy control were downloaded from the Gene Expression Omnibus database. Venn diagram, principal component analysis, heat map, volcano map, gene set enrichment analysis, gene ontology, and Kyoto encyclopedia of genes and genomes were used to analyze the data. Synovial tissue was identified as the key research objects. Further by protein–protein interaction network analysis of the four synovial tissue datasets and validation with immunohistochemistry of patients with RA and collagen-induced arthritis mice models, we identified that SLAMF8 may be a key biomarker for RA.

This study aims to assess the causal association between Interferon-γ (IFN-γ), IFN-γ receiver α (IFN-γR1), IFN-γ receiver β (IFN-γR2) and Systemic lupus erythematosus (SLE) within a bidirectional Mendelian-randomization design. Bidirectional two-sample MR was performed using inverse variance weighting (IVW), MR-Egger regression, and weighted median methods. A series of sensitivity analyses were conducted to assess the robustness of the results. Our study provides new insights into the role of IFN-γ, IFN-γR1, and IFN-γR2 in the treatment of SLE.