Autophagy and the redox connection: Virtual collection Vol 2

The Nobel Prize of Physiology or Medicine for 2016 has been awarded to Yoshinori Ohsumi for his discoveries of the mechanisms of autophagy. The phenomenon of autophagy was first observed in the 1950-60s in a series of elegant experiments showing cellular content being captured by lysosomes, degraded and recycled. In the 1980-90s, Yoshinori Ohsumi used powerful yeast genetic approaches to identify the genes involved in this process. This seminal work laid the foundation for the exponential growth in this field demonstrating that autophagy is involved not only in the starvation response but also in normal physiology. These findings are clinically important since perturbation of autophagy is linked to several diseases related to metabolism including Parkinson’s disease, diabetes and cancer. Interestingly, all of these pathologies involve changes in redox biology and the journal has presented cutting edge research in this area since its foundation in 2011. The redox biology of proteotoxicity is now an established focus and highly cited focus area for the journal. In this updated virtual collection on autophagy and proteotoxicity we highlight some of these recent developments featured in publications from Redox Biology including a co-authored paper by Dr Ohsumi (see new concepts below). The articles cover the redox regulation of autophagy, contribution of autophagy to redox signaling and damage, as well as reviews regarding autophagy regulation and diseases in a wide range of organs. We also include an educational overview suitable for adaptation for an advanced graduate course in autophagy and redox biology. SEND US YOUR PAPERS ON AUTOPHAGY AND PROTEOTOXICITY. Your article is likely to be widely read and the journal offers excellent service to authors with a 2016 impact factor of 6.235 and time to final decision under 3 weeks. As an Open Access journal you can access all these papers right now! The Autophagy Collection in Redox Biology: Original research 1. Chen W, Zou P, Zhao Z, Chen X, Fan X, Vinothkumar R, Cui R, Wu F, Zhang Q, Liang G and Ji J. Synergistic antitumor activity of rapamycin and EF24 via increasing ROS for the treatment of gastric cancer. Redox Biology. 2016; 10:7 8–89. 2. Garoby-Salom S, Rouahi M, Mucher E, Auge N, Salvayre R and Negre-Salvayre A. Hyaluronan synthase-2 upregulation protects smpd3deficient fibroblasts against cell death induced by nutrient deprivation, but not against apoptosis evoked by oxidized LDL. Redox biology. 2015; 4: 118–126. 3. Sklirou AD, Ralli M, Dominguez M, Papassideri I, Skaltsounis AL and Trougakos IP. Hexapeptide-11 is a novel modulator of the proteostasis network in human diploid fibroblasts. Redox Biol. 2015; 5: 205–15. 4. Yang S, Xia C, Li S, Du L, Zhang L and Zhou R. Defective mitophagy driven by dysregulation of rheb and KIF5B contributes to mitochondrial reactive oxygen species (ROS)-induced nod-like receptor 3 (NLRP3) dependent proinflammatory response and aggravates lipotoxicity. Redox biology. 2014; 3: 63–71. 5. Niforou K, Cheimonidou C and Trougakos IP. Molecular chaperones and proteostasis regulation during redox imbalance. Redox biology. 2014; 2:323–332. 6. Bansal S, Biswas G and Avadhani NG. Mitochondria-targeted heme oxygenase-1 induces oxidative stress and mitochondrial dysfunction in macrophages, kidney fibroblasts and in chronic alcohol hepatotoxicity. Redox Biol. 2014; 2:2 73–83. 7. Manley S, Ni H-M, Williams JA, Kong B, DiTacchio L, Guo G and Ding W-X. Farnesoid X receptor regulates forkhead Box O3a activation in ethanol-induced autophagy and hepatotoxicity. Redox biology. 2014; 2: 991–1002. 8. Wu D and Cederbaum AI. Inhibition of autophagy promotes CYP2E1-dependent toxicity in HepG2 cells via elevated oxidative stress, mitochondria dysfunction and activation of p38 and JNK MAPK. Redox biology. 2013; 1: 552–565. 9. Salabei JK and Hill BG. Mitochondrial fission induced by platelet-derived growth factor regulates vascular smooth muscle cell bioenergetics and cell proliferation. Redox biology. 2013; 1: 542–551.