**6. Concluding remarks**

Celiac disease is an increasingly complex disease, with a well-established genetic background but with a plethora of molecular/cellular actors involved. Despite this emerging complexity, the cellular uptake of the digested gliadin components and their ultimate fate is the key determinant for this disease. Once within a cell, gliadin peptides, as with any exogenous components, undergo different catabolic processes, including the relatively low-energy consumption processes such as exocytosis. In this scenario, autophagy protein turnover might represent a pro-survival process to counteract a surge in potentially toxic gliadin. However, for reasons still unknown, the autophagy process seems to be impaired in the celiac condition: as a result, gliadin is easily internalized in different types of cells, but no marked signs of a prominent degradation are reported. On the other hand, more and more is being learned about the process of autophagy and its molecular players, and, consequently, a relatively large number of molecular and pharmacological modulators are being put on the market and assayed in clinical trials for different pathologies. Therefore, once the alterations of the steady-state status of the autophagy process are clarified by comparing physiological to celiac pathological conditions, one could realistically hope to counteract gliadin toxicity by improving its catabolism within the cells, bearing in mind however

that the exacerbation of the fine autophagy intracellular balance might also lead to other, even more complex pathological conditions such as cancers.

This article focuses on the results of researches carried out by authors in the field of celiac disease.

It is of the upmost importance to investigate new therapeutic options for celiac patients, especially non-dietary therapies, in order to improve their quality of life.
