John Varga

This study identifies conserved fibroblast subsets and fibrotic mechanisms in osteoarthritis and systemic sclerosis using single-cell RNA-seq and spatial transcriptomics.

This paper identifies BLR-200, a CCN3-derived peptide, as an anti-fibrotic agent that impairs YAP activation and reduces bleomycin-induced skin fibrosis by blocking Sfrp2-positive fibroblast generation.

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

This study identifies ciliary program imbalance as a driver of fibroblast-to-myofibroblast reprogramming in systemic sclerosis, suggesting ciliotherapy as a potential treatment.

This study investigates the role of IL-23 in systemic sclerosis (SSc) and shows that tildrakizumab reduces fibrosis in experimental models.

The paper shows that altering primary cilia length in fibroblasts can reduce fibrotic responses across different fibrotic conditions.

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.

This study identifies Spag17 as a key modulator of female reproductive aging, showing its role in maintaining fertility and preventing age-related complications.

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.