Cdc42 small GTPase is a novel regulator of the fibrogenic activation of human intestinal myofibroblasts

Knockdown of CDC20 attenuates pulmonary fibrosis by repressing fibroblast activation via the TSC1-mediated mTOR pathway.

Idiopathic pulmonary fibrosis (IPF) is a fatal disease of the fibrous lungs that is closely associated with fibroblast activation. Cell division cycle protein 20 homolog (CDC20) regulates cell cycle progression, yet its role in lung fibrosis remains unclear. This study aimed to explore the function of CDC20 in IPF and...

Endocan Participates in TGF-β/Smad and AKT/ERK Signaling Coordination and lncRNA Modulation in Human Cardiac Fibroblasts

Findings indicate that endocan is required for the coordinated activation of canonical and non-canonical TGF-β signaling during fibroblast transdifferentiation and suggest its potential involvement in the molecular mechanisms underlying cardiac fibrosis.

Roflumilast Inhibits Fibrogenic Activation in Human Intestinal Myofibroblasts via Inhibition of Myocardin-Related Transcription Factor/Serum Response Factor Signaling

Findings indicate that PDE4 inhibitors, particularly roflumilast, effectively suppress TGF-β1-induced fibrogenic activation in HIMFs by modulating MRTF/SRF and Smad-dependent pathways, highlighting the value of roflumilast for further preclinical investigation as a potential therapeutic strategy for intestinal fibrosis...

autophagy regulates the phenotype and behavior of vascular smooth muscle cells

Noncanonical role for Caspase-5 in the human intestinal epithelium 2267092

The findings reveal that a select developmental isoform of CASP5 amplifies a key epithelial growth program, peaking in specific cell subsets in the intestinal epithelium to sustain their proliferation during stages critical of intestinal epithelial differentiation and regeneration.

Aberrant expression of the PREX2-MAGI2 axis modulates myofibroblast differentiation in pulmonary fibrosis.

It is suggested that MAGI2 acts as a negative regulator of myofibroblast differentiation by stabilizing PTEN, whereas PREX2 is aberrantly expressed in the fibrotic milieu, negatively modulating MAGI2, thereby accelerating pulmonary fibrosis.