As NKX2-5 is a dosage-sensitive regulator, we have speculated that changed NKX2-5 levels may mediate CHD development by influencing cardiac gene regulatory network.
Recent clinical and animal studies identified candidate mechanisms that may mediate the development of cardiovascular alterations in the setting of IUGR consistent with the hypothesis of perinatal programming [11, 12].
These results indicate that PVT1 may mediate the development and progression of diabetic nephropathy through mechanisms involving ECM accumulation.
The findings suggest that phenotypes related to subjective experiences upon smoking experimentation may mediate the development of nicotine dependence.
Lastly, we provide an overview of the current available treatments for advanced prostate cancer, considering where EVs may mediate the development of resistance against these drugs.
Collectively, these findings suggest that the loss of p53 expression during aging may mediate the development of cancer in an aging-dependent manner.
Based on combined information from studies of genetics, development, mouse models, and positive selection, several genes, including GTPBP6, IL3RA, RAI1, and UFD1L, can be highlighted as especially strong candidates for single genes whose altered expression may mediate the development of autistic and psychotic spectrum conditions, and social cognition more generally.
Experimental information suggests that UA may mediate the development of both hypertension and renal disease by dysfunction of endothelial and vascular smooth muscle cells resulting in oxidative stress, a reduction in endothelial nitric oxide, and activation of the renin-angiotensin system (15).
This would explain the changes in IL-6 secretion with advancing age and pose a potential mechanism through which increased IL-6 signalling may mediate MM growth and development.
Although PIF4 regulation of auxin biosynthesis presents a potential mechanism by which light may mediate changes in stomatal development, this requires further work.
