Key result
BRCC3 modulates BMP/TGF-β-PPARγ signaling, potentially driving vascular remodeling in pulmonary arterial hypertension.
Why the study?
The role of BRCC3 in modulating posttranslational modifications of BMP/TGF-β signaling pathways and its implication in pulmonary vascular remodeling in PAH is not well understood.
An imbalance of antiproliferative BMP (bone morphogenetic protein) signaling and proliferative TGF-β (transforming growth factor-β) signaling is implicated in the development of pulmonary arterial hypertension (PAH). The posttranslational modification (eg, phosphorylation and ubiquitination) of TGF-β family receptors, including BMPR2 (bone morphogenetic protein type 2 receptor)/ALK2 (activin receptor-like kinase-2) and TGF-βR2/R1, and receptor-regulated Smads significantly affects their activity and thus regulates the target cell fate. BRCC3 modifies the activity and stability of its substrate proteins through K63-dependent deubiquitination. By modulating the posttranslational modifications of the BMP/TGF-β-PPARγ pathway, BRCC3 may play a role in pulmonary vascular remodeling, hence the pathogenesis of PAH.
No takes yet. Share an insight, caveat, or question.
Shen et al. (2024) conducted a review in Pulmonary arterial hypertension (PAH). BRCC3 was evaluated. BRCC3 may play a role in pulmonary vascular remodeling and the pathogenesis of pulmonary arterial hypertension by modulating posttranslational modifications of the BMP/TGF-β-PPARγ pathway.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: