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Furthermore, mice made diabetic by streptozotocin (STZ) administration, but genetically deficient for the GcgR, display normal glucose tolerance [49]
231,232 These modifications alter gene expression and protein function, causing vascular dysfunction, inflammation, and oxidative stress, all of which contribute to the pathogenesis of DPN
Ongoing research continues to explore its activity in cellular communication and peptide signaling using controlled experimental models
Proc Natl Acad Sci USA 105(40):1557015575 Biojone C, Casarotto PC, Joca SR, Castrn E (2015) Interplay between nitric oxide and brain-derived neurotrophic factor in neuronal plasticity
Beyond the canonical SMAD pathway, TGF- also signals through non-SMAD mechanisms
10.1161/CIRCULATIONAHA.107.739938
