Channel opening probability (Po) of ENaCs is regulated by several physical and chemical factors.
Another factor that affects Po of ENaCs is a mechanical force.
ENaCs are critical in proliferation and differentiation of osteoblasts because ENaCs activate the expression of runt-related transcription factor 2 (RUNX2), a key transcriptional modulator of osteoblasts formation which plays a fundamental role in osteoblasts maturation and homeostasis.[sup] Furthermore, RUNX2 controls transcription of ossify-specific genes including OCN, OPN, and collagenase-3 in BMSCs and osteoblasts.
As discussed above, the activation of ENaCs triggers influx of sodium iron leading to a consequence that membrane potential is elevated temporarily.
Furthermore, urinary protein excretion is the cause of the renal abundance of ENaC subunits via regulatory Sgk1 [29, 30].
Furthermore, PAN-induced nephrotic syndrome correlates with sodium retention, decreased urinary excretion of sodium, marked ascites, and upregulation of protein levels of specific ENaC subunits .
It has recently been reported that there is an increase of ENaC activation in the kidney in PAN-induced nephrosis .
The second implication is that the reduced edema observed with WPC occurs via inhibition of ENaC activation.
In addition, CFTR regulates the activity of ENaC. ENaC interact with CFTR, CFTR could down-regulate ENaC in physiological conditions and compromise the function of ENaC.
CFTR and ENaC, as an important channel for epithelial fluid and electrolyte transport, play a key role in the AHR diseases.
One mechanism of atomization inhalation drug therapy is increasing the expression of ENaC. The current flow in intracellular Cl[sup]− channel not only guarantees H[sup]+-ATPase electrically neutral transport in the lacuna of some cell but also is very important for regulating cell capacity.
ENaC is distributed in cavity roof membrane in epithelial cells in all levels of the respiratory tract (from the nasopharynx to bronchioles).