EditorialTransautophagy: Research and Translation ofAutophagy Knowledge

Maria C. Albertini ,1 Tassula Proikas-Cezanne ,2,3 Nikolai Engedal ,4 Eva Žerovnik ,5

and Jon D. Lane 6

1University of Urbino “Carlo Bo”, Urbino, Italy2Eberhard Karls University of Tübingen, Tübingen, Germany3International Max Planck Research School “From Molecules to Organisms”, Tübingen, Germany4University of Oslo, Oslo, Norway5Jožef Stefan Institute, Ljubljana, Slovenia6University of Bristol, Bristol, UK

Correspondence should be addressed to Maria C. Albertini; maria.albertini@uniurb.it

Received 12 March 2018; Accepted 13 March 2018; Published 16 May 2018

Copyright © 2018Maria C. Albertini et al. This is an open access article distributed under the Creative Commons AttributionLicense, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work isproperly cited.

There is an urgent need to understand the process of autoph-agy in health and disease. Increasingly, human age-relateddiseases, such as cancer and neurodegeneration, as well asthe great variety of metabolic disorders are found to correlatewith significant alterations in both autophagy activity andcapacity. However, implementing novel therapeutic treat-ment opportunities for combatting age-related humanpathologies by targeting autophagy is unsatisfactorily slow.One of the reasons for this is that autophagy methods thatcan precisely monitor autophagy activity and capacityin vivo are currently nonexistent. Moreover, moleculardetails with regard to the complex regulation of autophagyin health and disease are still poorly understood. As a conse-quence, applying personalized medicine for targetingautophagy in patients suffering from age-related human dis-eases is still an unfulfilled aim.

In recognition of the requirement for developingnext-generation autophagy knowledge and methodologies,the COST (European Cooperation in Science andTechnology) Action (CA15138) “Transautophagy” (http://cost-transautophagy.eu/), a European network for multidis-ciplinary research on autophagy, has been successfully estab-lished by Caty Cases Louzao, Spain, and Patrice Codogno,France, in 2016. More than 200 autophagy researchers from

over 28 European and neighboring countries aim to signifi-cantly advance autophagy research, concentrating on basicresearch on the autophagy molecular machinery (workinggroup 1), strategies for autophagy analyses and modulation(working group 2), autophagy applications to crop andenergy production (working group 3), biomedical research(working group 4), and biomedical translation and clinicaltrials (working group 5).

In this special issue, important further information onmolecular mechanisms regulating autophagy is provided.These mechanisms highlight the relationship existingbetween cellular ROS levels and the process of autophagy.M. Pajares et al. reviewed publications related to the roleof redox signaling in autophagy regulation with a specialinterest on ageing-associated changes and Alzheimer’s dis-ease. J. Jin et al. used primary acute myeloid leukemia(AML) patient samples and human AML cell lines toinvestigate the requirement for autophagy in AML differ-entiation. They suggested that granulocytic AML differen-tiation relies on noncanonical autophagy pathways andthat restoring autophagic activity may be beneficial intherapies that aim at stimulating differentiation. N. Engedalet al. described novel aspects of oxidative stress-modulated miRNAs and elegantly demonstrated how an

HindawiOxidative Medicine and Cellular LongevityVolume 2018, Article ID 7504165, 3 pageshttps://doi.org/10.1155/2018/7504165

in silico approach can be employed to formulatehypotheses-driven research on the interrelation betweenmiRNA-based gene regulation, oxidative stress signalingpathways, and autophagy. T. Zuleger et al. investigatedthe role of the serum- and glucocorticoid-induced proteinkinase 1 (SGK1) in the control of autophagy. Their datastrongly support the idea that SGK1 inhibits the processof autophagy. SGK1 seems to act upstream of ULK1 inregulating autophagy, and the authors provide a modelwhereby SGK1 regulates autophagy by contributing tothe control of ULK1 gene expression. R. Mancinelli et al.reviewed the multifaceted roles of GSK-3 in cancer andautophagy-related diseases, in the context of the role ofGSK-3 in several signaling pathways controlling a greatvariety of different key cellular functions.

Polyphenols, and other antioxidant molecules, havebeen considered as compounds that modulate the processof autophagy. M. Holczer et al. investigated the role ofepigallocatechin-3-gallate (EGCG), the major polyphenolof green tea, in promoting autophagy-dependent survival.Their findings, obtained using HEK293T cells in vitro,revealed that EGCG treatment induced cytoprotectiveautophagy and increased cell viability by downregulatingmTOR and upregulating AMPK signaling. S. Hasanbašićet al. showed that a set of polyphenolic antioxidants, inparticular curcumin, can combat the process of proteinaggregation in vitro. However, some antioxidants, such asvitamin C and NAC may have opposing effects at higherconcentrations. The authors suggest that the level of pro-tein aggregation may act as a sensor in order to ultimatelyprevent further cellular damage. C. Miceli et al. explored the

effects of OA (Oleuropein aglycone, the main polyphenolfound in olive oil) in cardiomyocytes by overexpressionof monoamine oxidase-A (MAO-A). The authors observedthat OA treatment counteracted the cytotoxic effects ofMAO-A by restoring the MAO-A-induced defect inautophagic flux, most probably via activation and nucleartranslocation of TFEB (transcription factor EB).

Finally, further studies focused on the role of oxida-tive stress and autophagy in different pathologies andnew therapeutic strategies. M. Marinkovic et al. summa-rized the current knowledge of the interplay between autoph-agy regulation and five of the most life-threatening andprevalent malignancies (pancreatic, breast, hepatocellular,colorectal, and lung cancer). In addition, the authorspresent an overview of the recent advances in therapeu-tic strategies involving autophagy modulators in cancertherapy. A. Van Erp et al. reviewed knowledge on the cross-talk regulation between oxidative stress and autophagy inthe context of transplantation medicine. C. Fang et al. dis-cussed the implication of ROS and autophagy in both theonset and development of neurological disorders. Theauthors highlighted the interplay between ROS and autoph-agy in establishing a determinant role in the modulation ofneuronal homeostasis, by an as yet unexplored mechanism,important in cerebral ischemia, AD (Alzheimer’s disease),and PD (Parkinson’s disease).

In summary, this special issue provides several newaspects in autophagy research with emphasis on transla-tion of knowledge to applications, critically including thetopic of autophagy regulation upon oxidative stress, aging,age-related diseases, and beyond (Figure 1).

Signal controlof autophagy

miRNAsSGK1

(i)(ii)

(iii)(iv)(v)

(vi)

GSK-3EGCGCurcumin

Autophagy and ROS

Autophagyand Cancer

AML(i)(ii) HCC, breast,

lung, pancreatic,and colorectalcancer

Autophagyand

transplantationmedicine

Autophagyand

neurodegeneration

Oleuropeinaglycone

Figure 1: Summary of topics that either have been discussed in review articles or have been addressed in original studies in this special issue.

2 Oxidative Medicine and Cellular Longevity

Acknowledgments

We wish to thank all the authors and reviewers whoparticipated in this issue. We acknowledge the COSTAction (CA15138) “Transautophagy” for providingfinancial support.

Maria C. AlbertiniTassula Proikas-Cezanne

Nikolai EngedalEva ŽerovnikJon D. Lane

3Oxidative Medicine and Cellular Longevity

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