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Fig. 5 | Stem Cell Research & Therapy

Fig. 5

From: The functional mechanism of bone marrow-derived mesenchymal stem cells in the treatment of animal models with Alzheimer’s disease: crosstalk between autophagy and apoptosis

Fig. 5

Interaction between autophagy and apoptosis. The downregulation of autophagy causes neural apoptosis. Autophagy is able to accelerate apoptosis via the degradation of IAPs as well. Apoptosis inhibits autophagy in enzyme-dependent manners. There is signal crosstalk between apoptosis and autophagy by sharing common regulators such as p53, Atg5, caspase-8, Beclin-1/Bcl-2, and IAPs. IAPs, inhibitors of apoptosis proteins; Bcl-2, B-cell lymphoma 2; Cyto c, cytochrome c; c-FLIP, cellular FLICE-like inhibitory protein; PIP3, phosphatidylinositol 3,4,5-trisphosphate; PI3K, phosphatidylinositol 3-kinase; PTEN, phosphatase and tensin homolog; AKT or PKB, protein kinase B; mTOR, mammalian target of rapamycin; ATG5, autophagy related 5; LC3, microtubule-associated proteins 1A/1B light chain 3B; p53, tumor protein P53; NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells

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