Are mammalian target of Rapamycin inhibition and mycobacterial survival uncoupled in murine macrophages?
This data, coupled with previous work from our laboratory, further indicates that autophagy induction by mTOR inhibition is an artificial means to increase mycobacterial killing and masks more relevant endogenous autophagic biochemistry that needs to be understood.
BM-MSCs could alleviate the renal damages of adenine-induced CRF, reduce the excretion of proteinuria, increase the glomerular capillaries density, promote the secretion of VEGF and finally contribute to improve renal function. VEGF-induced angiogenesis is mediated through activating PI3k-Akt signaling pathway.