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Review
. 2022 Aug 5:13:903836.
doi: 10.3389/fendo.2022.903836. eCollection 2022.

Autophagy in aging-related oral diseases

Daniel Peña-Oyarzún  1   2   3 , Carla San Martin  2 , María Paz Hernández-Cáceres  3 , Sergio Lavandero  4   5   6 , Eugenia Morselli  7   8 , Mauricio Budini  3   8 , Patricia V Burgos  8   9   10   11 , Alfredo Criollo  3   4   8
Affiliations
Review

Autophagy in aging-related oral diseases

Daniel Peña-Oyarzún et al. Front Endocrinol (Lausanne). .

Abstract

Autophagy is an intracellular degradation mechanism that allows recycling of organelles and macromolecules. Autophagic function increases metabolite availability modulating metabolic pathways, differentiation and cell survival. The oral environment is composed of several structures, including mineralized and soft tissues, which are formed by complex interactions between epithelial and mesenchymal cells. With aging, increased prevalence of oral diseases such as periodontitis, oral cancer and periapical lesions are observed in humans. These aging-related oral diseases are chronic conditions that alter the epithelial-mesenchymal homeostasis, disrupting the oral tissue architecture affecting the quality of life of the patients. Given that autophagy levels are reduced with age, the purpose of this review is to discuss the link between autophagy and age-related oral diseases.

Keywords: aging; autophagy; oral cancer; oral diseases; periapical lesions; periodontitis.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Autophagic pathway. The autophagosome is a double membrane organelle which sequesters intracellular material. Then, the autophagosome fuses with the lysosome to form the autolysosome where hydrolytic enzymes promote the degradation of the autolysosome cargo. The catabolism of the cargo generates simple new metabolites that turn back to the cytosol to be used in different metabolic pathways.
Figure 2
Figure 2
The autophagic machinery. Different types of stressors can be sensed by MTOR and AMPK. MTOR inhibits the ULK1 complex kinase activity phosphorylating its Ser757. Under stress conditions, AMPK activates ULK1 by phosphorylation on Ser317, Ser555, and Ser777, leading to the activation of the class III phosphatidylinositol 3-phosphate kinase complex (PtdIns3KC3). Then, active PtdIns3KC3 increases the levels of phosphatidylinositol 3-phosphate (PtdIns3P) in specific membrane micro domains, allowing the recruitment of proteins like the WD repeat domain, phosphoinositide interacting (WIPI). Thus, elongation of the phagophore membrane is mediated by two ubiquitination-like systems: the complex ATG12-ATG5-ATG16 and the conjugate LC3-phosphatidylethanolamine (PE), known as LC3-II. Additionally, both ATG2 and ATG9 participate in the elongation of the autophagosome through the trafficking of lipids from the endoplasmic reticulum or the Golgi apparatus. Once that the autophagosome membrane engulf intracellular components it encloses itself and then fuses with lysosomes to form the autolysosome. Chloroquine (CQ) or bafilomycin A1 (BafA1) can be used to block autophagosome-to-lysosome fusion, allowing the accumulation of autophagosomes.
Figure 3
Figure 3
Autophagy and age-related oral diseases. Aging is a physiological process in which different cellular mechanism decline, leading in most of cases age-related diseases. “Autophagy”, which is impaired during aging, has been shown be critical to the control of age-related oral diseases such as oral cancer, periodontitis and periapical lesions.
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