Targeting αvβ8 Integrin with Monoclonal Antibody MEDI8367 Prevents Fibrosis in Preclinical Models of CKD.
Baker, David et al.
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#FibrosisResearch #CKD #αvβ8inhibition

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FIBROTARGET partners will be there to discuss the latest in fibrosis innovation and patient-centred trial design. Don’t miss the opportunity to connect and explore how we’re advancing research in intestinal fibrosis!

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Antibody Treatment Could Block Gut-Derived Toxin Behind Kidney Fibrosis A gut microbe molecule drives diabetic kidney scarring. Blocking it may offer new treatment options. A new study from the University of Illinois Urbana-Champaign and Mie University in Japan has revealed...

Antibody Treatment Could Block Gut-Derived Toxin Behind Kidney Fibrosis #Science #HealthandMedicine #InfectiousDiseases #KidneyHealth #AntibodyTreatment #FibrosisResearch

Cereno’s IPF drug clears Phase I, paving way for Phase II The company plans to start Phase II trial for HDAC inhibitor CS014 as a treatment for idiopathic pulmonary fibrosis (IPF) in H1 2026.

Armed with positive topline results from its Phase I trial, Cereno plans to start Phase II trial for HDAC inhibitor CS014 as a treatment for idiopathic pulmonary fibrosis (IPF) in H1 2026.

#news #CerenoScientific #CS014 #FibrosisResearch #IPF #PulmonaryFibrosis #ClinicalTrials #BiotechNews

Cereno’s IPF drug clears Phase I, paving way for Phase II The company plans to start Phase II trial for HDAC inhibitor CS014 as a treatment for idiopathic pulmonary fibrosis (IPF) in H1 2026.

Armed with positive topline results from its Phase I trial, Cereno plans to start Phase II trial for HDAC inhibitor CS014 as a treatment for idiopathic pulmonary fibrosis (IPF) in H1 2026.

#news #CerenoScientific #CS014 #FibrosisResearch #IPF #PulmonaryFibrosis #ClinicalTrials #BiotechNews

RUNX2 promotes fibrosis via an alveolar-to-pathological fibroblast transition | Nature A hallmark of pulmonary fibrosis is the aberrant activation of lung fibroblasts into pathological fibroblasts that produce excessive extracellular matrix1–3. Thus, the identification of key regulators that promote the generation of pathological fibroblasts can inform the development of effective countermeasures against disease progression. Here we use two mouse models of pulmonary fibrosis to show that LEPR+ fibroblasts that arise during alveologenesis include SCUBE2+ alveolar fibroblasts as a major constituent. These alveolar fibroblasts in turn contribute substantially to CTHRC1+POSTN+ pathological fibroblasts. Genetic ablation of POSTN+ pathological fibroblasts attenuates fibrosis. Comprehensive analyses of scRNA-seq and scATAC-seq data reveal that RUNX2 is a key regulator of the expression of fibrotic genes. Consistently, conditional deletion of Runx2 with LeprcreERT2 or Scube2creERT2 reduces the generation of pathological fibroblasts, extracellular matrix deposition and pulmonary

RUNX2 drives fibrosis by transforming LEPR+ fibroblasts into pathological ones in pulmonary fibrosis models. Key insights for new therapies! #FibrosisResearch PMID:39910313, Nature 2025, @Nature https://doi.org/10.1038/s41586-024-08542-2 #Medsky #Pharmsky #RNA #ASHG #ESHG 🧪