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

Endocan, a soluble dermatan sulfate proteoglycan, is increasingly recognized as a regulator of key cellular pathways in both physiological and pathological contexts. While TGF-β is a central mediator of fibrotic remodeling, the role of endocan in this process remains elusive. By performing a transcriptomic dataset anal...

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

The lack of effective anti-fibrotic agents remains a significant unmet need in the treatment of intestinal fibrosis, a condition largely driven by transforming growth factor-β1 (TGF-β1)-mediated myofibroblast activation. Phosphodiesterase 4 (PDE4) inhibitors, known to increase intracellular cAMP levels, exhibit anti-in...

autophagy regulates the phenotype and behavior of vascular smooth muscle cells

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

Caspase-5 (CASP5) is a member of the inflammatory caspase family of cysteine proteases involved in inflammation and cell death. CASP5 shares highest homology with inflammatory caspase-4, but while caspase-4 is essential for noncanonical inflammasome activation, CASP5 is generally dispensable. This conundrum has l...

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.