Systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) are two common multisystem autoimmune diseases that share, among others, many clinical manifestations and serological features. The role of long non-coding RNAs (lncRNAs) has been of particular interest in the pathogenesis of autoimmune diseases. Here, we aimed to summarize the roles of lncRNAs as emerging novel biomarkers and therapeutic targets in SLE and RA. We conducted a narrative review summarizing original articles on lncRNAs associated with SLE and RA, published until November 1, 2021. Based on the studies on lncRNA expression profiles in samples (including PBMCs, serum, and exosomes), it was noted that most of the current research is focused on investigating the regulatory mechanisms of these lncRNAs in SLE and/or RA. Several lncRNAs have been hypothesized to play key roles in these diseases. In SLE, lncRNAs such as GAS5, NEAT1, TUG1, linc0949, and linc0597 are dysregulated and may serve as emerging novel biomarkers and therapeutic targets. In RA, many validated lncRNAs, such as HOTAIR, GAS5, and HIX003209, have been identified as promising novel biomarkers for both diagnosis and treatment. The shared lncRNAs, for example, GAS5, may participate in SLE pathogenesis through the mitogen-activated protein kinase pathway and trigger the AMP-activated protein kinase pathway in RA. Here, we summarize the data on key lncRNAs that may drive the pathogenesis of SLE and RA and could potentially serve as emerging novel biomarkers and therapeutic targets in the coming future.

Venous thromboembolism is a condition that includes deep vein thrombosis and pulmonary embolism. It is the third most common cardiovascular disease behind acute coronary heart disease and stroke. Over the past few years, growing research suggests that venous thrombosis is also related to the immune system and inflammatory factors have been confirmed to be involved in venous thrombosis. The role of inflammation and inflammation-related biomarkers in cerebrovascular thrombotic disease is the subject of ongoing debate. P-selectin leads to platelet-monocyte aggregation and stimulates vascular inflammation and thrombosis. The dysregulation of miRNAs has also been reported in venous thrombosis, suggesting the involvement of miRNAs in the progression of venous thrombosis. Plasminogen activator inhibitor-1 (PAI-1) is a crucial component of the plasminogen-plasmin system, and elevated levels of PAI-1 in conjunction with advanced age are significant risk factors for thrombosis. In addition, it has been showed that one of the ways that neutrophils promote venous thrombosis is the formation of neutrophil extracellular traps (NETs). In recent years, the role of extracellular vesicles (EVs) in the occurrence and development of VTE has been continuously revealed. With the advancement of research technology, the complex regulatory role of EVs on the coagulation process has been gradually discovered. However, our understanding of the causes and consequences of these changes in venous thrombosis is still limited. Therefore, we review our current understanding the molecular mechanisms of venous thrombosis and the related clinical trials, which is crucial for the future treatment of venous thrombosis.

Systemic lupus erythematosus (SLE) is a complex autoimmune disease marked by abnormal B-cell proliferation and increased autoantibodies. miRNAs play a crucial role in regulating B-cell dysfunction and SLE pathology. miRNAs influence DNA methylation, B-cell activation, and gene expression, contributing to SLE pathogenesis. miRNAs impact B cells through key processes like proliferation, differentiation, tolerance, and apoptosis. miRNAs also exacerbate inflammation and immune responses by modulating Interleukin 4 (IL-4), IL-6, and interferon cytokines. Autophagy, a key degradation mechanism, is also regulated by specific miRNAs that impact SLE pathology. This article explores the role of multiple miRNAs in regulating B-cell development, proliferation, survival, and immune responses, influencing SLE pathogenesis. miRNAs like miR-23a, the miR-17 ∼ 92 family, and miR-125b/miR-221 affect B-cell development by regulating transcription factors, signaling pathways, and cell cycle genes. miRNAs such as miR-181a-5p and miR-23a-5p are differentially regulated across developmental stages, emphasizing their complex regulatory roles in B-cell biology. This article synthesizes miRNA-B cell interactions to offer new strategies and directions for SLE diagnosis and treatment.

Over the past few decades, the prevalence of hypervirulent Klebsiella pneumoniae (hvKp) in the Asia-Pacific region, notably associated with community-acquired pyogenic liver abscesses, has been alarming. Most existing hvKp detection methods are time-consuming and rely on expensive equipment, which is particularly problematic in resource-limited settings. Thus, there is an urgent need for convenient, rapid, and cost-effective approaches to the identification and quantification of hvKp. In this study, we developed a CRISPR Cas12a-based smartphone-assisted colorimetric quantitative platform (Cas12a-SACQP), a portable platform enabling visible nucleic acid detection and analysis via a smartphone application with on-site detection capability. We applied Cas12a-SACQP to detect multiple virulence genes of hvKp, including rmpA, iroB, iucA, and peg-344. The limits of detection (LODs) for these genes were 2.42 CFU/mL for rmpA, 2.33 CFU/mL for iroB, 1.72 CFU/mL for iucA, and 2.83 CFU/mL for peg-344, respectively. We simultaneously tested Klebsiella pneumoniae clinical strains from various samples (ear discharge, sputum, and blood) for these virulence genes. Compared with conventional PCR identification and real-time PCR, Cas12a-SACQP effectively differentiates classical Klebsiella pneumoniae (cKp) from hvKp from these diverse clinical sources. Furthermore, the entire Cas12a-SACQP workflow can be performed using portable devices, and the results can be rapidly visualized via a smartphone. This platform, therefore, holds substantial potential for rapid and quantitative detection of clinical pathogens in resource-constrained environments.