Systemic Sclerosis and Related Diseases

This study identifies AURKA/HDAC6 activation as a driver of primary cilia shortening and fibroblast activation in systemic sclerosis.

This study shows that some anti-topoisomerase 1 autoantibodies (ATAs) in systemic sclerosis (SSc) bind more strongly to TOP1-DNA cleavage complexes, correlating with disease severity and immune activation.

This study identifies neutrophil reprogramming in systemic sclerosis (SSc) driven by HMGB1+ extracellular vesicles, leading to lung inflammation and fibrosis, and suggests therapeutic targeting of HMGB1.

This study uses blood vessel organoids to model systemic sclerosis vasculopathy and fibrosis, showing that SSc serum induces epigenetic and molecular changes linked to endothelial dysfunction and potential therapeutic targets.

This paper identifies small molecules targeting the Tenascin C fibrinogen-like globe domain to reduce fibrosis in systemic sclerosis by inhibiting Toll-like receptor 4 signaling.

The paper uses spatial transcriptomic methods to identify novel fibroblast subpopulations in systemic sclerosis skin and their pathogenic roles.

This study compares cAMP regulation and dedifferentiation in lung and skin myofibroblasts from scleroderma patients, finding tissue-specific differences in PGE2 response and p38 inhibition effects.

The paper examines metabolic profiles of circulating plasmacytoid dendritic cells (pDCs) in systemic sclerosis (SSc) patients, finding differences based on clinical phenotypes.

This study identifies aging and senescence signatures in SSc-ILD through gene expression analysis and telomere length measurement, linking them to disease pathology.

This study shows that reducing PKD2 activity in mice prevents bleomycin-induced dermal fibrosis by decreasing collagen and inflammatory markers.

The paper uses RNA-Seq to analyze SSc patient and control samples, identifying SPAG17 and SOX9 non-coding RNAs as novel factors in SSc pathogenesis.

The paper identifies AREG as a critical driver of bleomycin-induced skin fibrosis and shows that targeting the AREG-EGFR-MEK pathway can prevent fibrosis.

The paper identifies differential DNA methylation in skin fibroblasts from African American systemic sclerosis patients, linking it to immune and metabolic pathways.

This study identifies a three-gene network influencing lung function and autoantibody status in systemic sclerosis patients through genetic interaction analysis.

The paper evaluates the antifibrotic effects of triple siRNA targeting SPARC, CCR2, and SMAD3 in a mouse model of fibrosis, showing reduced inflammation and fibrosis through multi-target intervention.

The paper performs a meta-analysis of gene expression data from SSc clinical trials to identify therapeutic targets and predict treatment response using machine learning.