CTGF (Connective tissue growth factor)

To overcome these limitations, we systematically evaluated the synergistic Combination effects of three drug candidates, OTX-015 (BET inhibitor), Metformin (metabolic regulator), and Anlotinib (multitargeted tyrosine kinase inhibitor), with Chidamide. Chidamide and Anlotinib synergistically inhibit Hippo signaling pathway, which reveals a novel "dual epigenetic kinase targeting" strategy for the treatment of T-ALL. Future studies should validate these findings in vivo and investigate the impact of the metabolic microenvironment on therapeutic efficacy.

STING deficiency alleviates scar formation after GFS by suppressing p38 MAPK pathway. Targeting STING/p38 axis may improve surgical outcomes by modulating the balance between inflammation and tissue repair.

These findings suggest that WMW intervention is associated with coordinated alterations in inflammation-related signaling, cell proliferation, and extracellular matrix remodeling in CRC, with focal adhesion-YAP-related mechanotransduction representing a potential associated feature. This study provides integrated experimental evidence supporting further investigation of WMW and traditional Chinese medicine-based strategies targeting focal adhesion-associated signaling in CRC research.

We developed a viable in vitro model to study contact-compression, showing biomechanical inflammatory and remodeling responses. With adjustable components, this model can be applied to further study tissue responses to lung implants.

However, adjuvant chemotherapy significantly led to better overall survival. The Hippo pathway is frequently deregulated (nuclear YAP/TAZ in 61.4% of patients), suggesting it is a compelling novel therapeutic target for this aggressive disease.

Results suggest that WISP1, a stroma-specific secreted protein, modulates the behavior of bladder stroma cells via autocrine signaling. WISP1 induces tumor growth of bladder carcinoma cells in an isoform-dependent manner via paracrine signaling, indicating that WISP1 may behave as a mediator linking diseases of the human bladder.

hAFSC-EVs treatment can help restore DMA-induced bladder dysfunction, which is associated with lowered blood glucose levels, reduced arterial wall thickness, and decreased TNF-α, IL-6, TGF-β1, Smad3, and CTGF expression.

Using CRISPR/Cas9-mediated knockout and rescue experiments in EOC cell lines, we demonstrate that MED12 deficiency significantly enhances sensitivity to ferroptosis inducers (RSL3 and Erastin), as evidenced by reduced IC50 values...Pharmacological inhibition of YAP with verteporfin or siRNA-mediated TEAD1 knockdown reverses ferroptosis sensitivity in MED12-deficient cells, confirming pathway specificity. These findings establish MED12 as a modulator of the YAP-TEAD1-ferroptosis axis and suggest that targeting this pathway could overcome chemoresistance in MED12-deficient EOC. Our work provides a mechanistic foundation for exploiting ferroptosis induction as a therapeutic strategy in ovarian cancer.

These compounds can ameliorate pulmonary inflammation, epithelial-mesenchymal transition, and collagen deposition through diverse immune mechanisms, acting at specific stages or throughout the fibrotic process, thereby supporting PF management. This review examines current scientific understanding of natural products' immunological effects in PF, which is crucial for developing future anti-PF therapeutics.

It was also determined that CYTOR suppression caused a decrease in the expression of the YAP1 gene, a key effector of the Hippo signaling pathway and the CTGF gene, one of its target genes. In conclusion, our findings suggest that CYTOR may be a potential therapeutic target in breast cancer by regulating the Hippo signaling pathway.

In this study, we investigated the anti-inflammatory and anti-invasive properties of 1,3,6-tri-O-galloyl-α-D-glucose (αTGG), the α-anomer of βTGG from Terminalia chebula, in comparison with pharmacological Hippo pathway inhibitors IAG933, VT107, and GNE7883...Importantly, αTGG and VT107 also significantly attenuated ConA-induced activation of proMMP-2 to MMP-2 and reduced the expression of multiple pro-inflammatory mediators, including COX2, CCL22, CCR2, CCR4, CXCL10, CXCL12, CXCR1, FASLG, IFNG, IL13, and IL17A. These findings underscore the dual anti-inflammatory and anti-invasive actions of αTGG, positioning it as a promising candidate for targeting inflammation-driven GBM progression through modulation of Hippo pathway activity.

18F-FAPI PET/CT imaging may hold promise for identifying active pulmonary fibrosis and monitoring its progression in pneumoconiosis, suggesting a potential clinical opportunity for targeted anti-fibrotic treatment. These preliminary findings warrant further investigation in larger studies.