Lipopolysaccharide released from gut activates pyroptosis of macrophages via Caspase 11-Gasdermin D pathway in systemic lupus erythematosus.

Noncanonical pyroptosis is triggered by Caspase 4/5/11, which cleaves Gasdermin D (GSDMD), leading to cell lysis. While GSDMD has been studied previously in systemic lupus erythematosus (SLE), the role of pyroptosis in SLE pathogenesis remains unclear and contentious, with limited understanding of Caspase 11-mediated pyroptosis in this condition. In this study, we explored the level of Caspase 11-mediated pyroptosis in SLE, identifying both the upstream pathways and the interaction between pyroptosis and adaptive immune responses.

Keratinocyte-to-macrophage communication exacerbate psoriasiform dermatitis via LRG1-enriched extracellular vesicles.

Macrophage-associated inflammation and keratinocytes excessive proliferation and inflammatory cytokines secretion induced by stimulation play an important role in the progression of psoriasiform dermatitis. However, how these two types of cells communicate remains obscure. We induced a mouse model with experimental psoriasiform dermatitis by Imiquimod (IMQ).

Effects of fecal microbiota transplant on DNA methylation in patients with systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a highly heterogeneous autoimmune disease characterized by multiple organ damage accompanied by the over-production of autoantibodies. Decreased intestinal flora diversity and disruption of homeostasis have been proven to be associated with pathogenesis of SLE. In previous study, a clinical trial was conducted to verify the safety and effectiveness of fecal microbiota transplantation (FMT) in the treatment of SLE.

Exploring the Complex Relationship Between Microbiota and Systemic Lupus Erythematosus.

Purpose Of Review: Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by various autoantibodies and multi-organ. Microbiota dysbiosis in the gut, skin, oral, and other surfaces has a significant impact on SLE development. This article summarizes relevant research and provides new microbiome-related strategies for exploring the mechanisms and treating patients with SLE.

Recent advances in systemic lupus erythematosus and microbiota: from bench to bedside.

Systemic lupus erythematosus (SLE) is a complicated autoimmune disease affecting multiple systems and organs. It is highly heterogeneous, and it preferentially affects women at childbearing age, causing worldwide social burden. The pathogenesis of SLE mostly involves genetic predisposition, epigenetic dysregulation, overactivation of the immune system, and environment factors.

NCAPD3 enhances Warburg effect through c-myc and E2F1 and promotes the occurrence and progression of colorectal cancer.

Background: NCAPD3 is one of the three non-SMC subunits of condensin II complex, which plays an important role in the chromosome condensation and segregation during mitosis. Notably, elevated levels of NCAPD3 are found in many somatic cancers. However, the clinical role, biological functions of NCAPD3 in cancers especially in colorectal cancer (CRC) and the underlying molecular mechanisms remain poorly elucidated.

Animal models of systemic lupus erythematosus and their applications in drug discovery.

Introduction: Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease with substantial phenotypic heterogeneity. Currently, our understanding of the pathogenesis is still limited, and as a result, specific and efficacious therapies are lacking. Various mouse models have been established to serve as powerful tools that will promote a better understanding of the disease and the ability to test novel drugs before clinical application.

NCAPD3 promotes prostate cancer progression by up-regulating EZH2 and MALAT1 through STAT3 and E2F1.

NCAPD3 is one of the non-SMC regulatory subunits of Condensin II, which is mainly responsible for the condensation and segregation of chromosomes during mitosis. However, its role in cancer especially in prostate cancer (PCa) and the molecular mechanism have not been clearly elucidated. Here, we find that NCAPD3 is high-expression and up-regulates the levels of EZH2 and MALAT1 in PCa.

Regulatory mechanism of androgen receptor on NCAPD3 gene expression in prostate cancer.

Background: Androgen receptor (AR) is an essential transcriptional factor that contributes to the development and progression of prostate cancer (PCa). NCAPD3 is a component of the condensin II complex and plays a critical role in cell mitosis by regulating chromosome condensation; however, the relationship between NCAPD3 and AR remains unknown.

Methods: Transcriptome sequencing assay is carried out to analyze the expression of the NCAP family in clinic samples.

Study on correlation between property of coronary artery lesion and degree of coronary artery stenosis of elderly patients with coronary heart disease.

Objective: To discuss the influence of coronary artery lesion of elderly patients with coronary heart disease (CHD) on left ventricular remodeling.

Methods: Retrospective selection method was used to choose 80 elderly CHD patients who received coronary angiogram examination in Baoding First Central Hospital from January 2014 to February 2018 as the objects of study. According to coronary artery lesion, the patients were classified into single vessel lesion group (single vessel group) and multi-vessel lesion group (multi-vessel group, the number of lesion vessels≧2).