ArticleCell death discovery2026
NRP1 promotes hepatic fibrosis by regulating Src/Rab7-mediated lysosomal degradation of TβRI.
Article in Cell death discovery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
BACKGROUND AND
aimsActivation of hepatic stellate cells (HSCs) and subsequent dysregulation of the TGF-β1 signaling pathway are central to the progression of hepatic fibrosis. Neuropilin-1 (NRP1) has been identified as a co-receptor involved in multiple signaling pathways, yet its role in modulating TGF-β receptor stability in HSCs remains to be fully elucidated. This study investigated the regulatory role of the NRP1/Src/Rab7 axis in TβRI lysosomal degradation during HSC activation.
methodsHepatic fibrosis was induced in male C57BL/6 mice via intraperitoneal CCl
resultsNrp1 silencing in primary HSCs reduced TβRI protein levels and attenuated p-Smad2/3 signaling without affecting mRNA levels. Consistently, NRP1 deficiency accelerated lysosomal degradation of TβRI, accompanied by increased TβRI-LAMP1 colocalization and enhanced trafficking of TβRI into Rab7-positive late endosomes. Mechanistically, NRP1 loss diminished Src kinase activity and consequently reduced Src-dependent tyrosine phosphorylation of Rab7, leading to elevated Rab7-GTP levels and enhanced late endosomal sorting of TβRI. Rab7 knockdown or Src reactivation partially rescued TβRI stability and restored downstream signaling. In vivo, HSC-specific Nrp1 knockdown attenuated CCl
conclusionsThese data suggest that the NRP1/Src/Rab7 axis contributes to TβRI stability by modulating its lysosomal degradation pathway. Targeting this axis may provide a potential approach for intervening in the progression of hepatic fibrosis.
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