It is possible that the quality control of myelin protein synthesis and cellular organelle development that are achieved by autophagy might be tightly associated with the myelination process or with SC differentiation. However, our results did not support this hypothesis, because the axonal sorting and initial myelination processes took place normally in atg7 knockout mice. In addition, we found that autophagy appears to be primarily activated when myelination is already in an advanced stage. It was recently reported that SC-specific mTOR null mice exhibited delayed myelination, indicating an important role for the mTOR pathway in SC myelination. Although autophagy may be enhanced or abnormally activated in mTOR-null mice, increased autophagy might not be responsible for the defect in myelination in this mutant. In consistency with this finding, it was found that the activation of autophagy with rapamycin during postnatal development did not alter normal myelination in vivo. Therefore, these findings suggest a distinct mechanistic regulation of the initiation of myelination and constitutive autophagy. Moreover, we have not found abnormally compacted myelin lamellae in the atg7-SCKO nerves at P10 and P60. This finding indicates that cytoplasmic exclusion from closely condensed myelin membranes during the growth of compacted myelin sheath is mainly performed by myelin protein interaction between closely apposed membranes, but is not BYL719 related to autophagic removal of cytoplasm. Unexpectedly, we have found the hypermyelination of small fibers in the atg7–SCKO mutant mice. The increased number of myelinated axons in mutant nerves, even though it was statistically insignificant, may be related to the hypermyelination potential of atg7–SCKO mutants. At this moment, we do not know how the loss of atg7 resulted in hypermyelination in adulthood. Excess residual cytoplasm in the mSCs of the mutant mice may or may not be related to these abnormalities. NCV of atg7–SCKO mutant mice was not accelerated compared to the control mice suggesting that the hypermyelination of small fibers does not significantly contribute to NCV. The increased amplitude of CMAP in atg7–SCKO mutant mice may be associated with mild increase of the number of myelinating axons. Further studies on the molecular mechanism of abnormal peripheral nerve function in atg7-SCKO mice are required. Heart failure is associated with activation of the renin-angiotensin system and sustained increased vasopressin release from the pituitary gland. RAS and AVP have been shown to play a role in the kidneys by taking part in the development of hyponatremia and water retention. Hyponatremia and water retention in HF is associated with a poor outcome. There is increasing evidence of a crosstalk between angiotensin II and AVP with potential enhancing effects on water retention mediated by renal water channels. We have previously demonstrated that rats with chronic HF 21 days after myocardial infarction increased the abundance of the renal water channel aquaporin-2 in the inner medullary collecting ducts.