PDGFRB (Platelet Derived Growth Factor Receptor Beta)

P2, N=70, Active, not recruiting, National Institute of Allergy and Infectious Diseases (NIAID) | Trial completion date: Mar 2026 --> Mar 2027

P1/2, N=20, Recruiting, Princess Maxima Center For Pediatric Oncology

Meanwhile, MSC-EVs induced heterogeneous responses. These findings establish MIA-EVs as a conditioning-resistant, systems-regulated, cell-free platform with regenerative, immunomodulatory, and cytoprotective potential under hostile microenvironments.

Enhancing pericyte maturity or intercepting transitions toward CAFs are promising avenues to boost treatment efficacy. We propose a practical framework for classifying "MSC-pericyte states" in the TME and emphasize rigorous, multi-marker, spatially resolved analyses to dissect their complex functions, thus opening a new scenario for targeted therapies.

P2, N=70, Active, not recruiting, National Institute of Allergy and Infectious Diseases (NIAID) | Recruiting --> Active, not recruiting

P2, N=10, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Dec 2025 --> Jan 2027

P2, N=53, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Jun 2026 --> Jan 2027

P2, N=98, Recruiting, UMC Utrecht | Trial completion date: Dec 2026 --> Dec 2027 | Trial primary completion date: Dec 2026 --> Dec 2027

HSYA, as a multi-target, multi-pathway natural bioactive compound, demonstrates significant potential in delaying liver fibrosis and preventing and treating liver cancer. In particular, HSYA exerts potent anti-fibrotic and anti-hepatocellular carcinoma effects by modulating key signaling pathways such as PPARγ, NF-κB, and PI3K/Akt. This mechanism likely represents the critical pathway through which HSYA effectively blocks the progression from fibrosis to HCC.

Tissue localization analysis with a PDGF-D reporter identified fibroblasts and endothelial cells as inflammation-responsive PDGF-D sources. These findings reveal evolutionarily divergent PDGF-D sensing mechanisms in ILC3s and uncover their differential contributions to mucosal immunity during infection.

Postoperative recovery was rapid; although soft feces persisted for one month, normal stool consistency was subsequently restored, and the patient achieved significant weight gain. This case underscores the diagnostic and therapeutic challenges associated with non-neoplastic, inflammation-driven SBO and suggests that activation of the PDGFR-β/FGFR pathways may play a key role in fibroplasia-related intestinal strictures, offering a novel molecular perspective beyond conventional SBO etiologies.

This study used three disease models: anti-glomerular basement membrane (anti-GBM) disease, Adriamycin nephropathy, and adenine-containing diets...We found FGF23-driven renal patterns of proinflammatory gene and protein expression or leukocyte overabundance. The present data provide evidence that excess FGF23 directly drives inflammation in kidney disease and may serve as a therapeutic target.