It has also been described the role of p53 tumor suppressor protein in regulating autophagy. In fact, depending on the p53 location, this protein exerts 
distinct and important function. Regarding this dual role, nuclear p53 acts as a transcription factor to stimulate both DRAM1 and Sestrin 2, which in turns switch on autophagy. In contrast, cytoplasmic p53 inhibits autophagy. In order to induce autophagy, p53 is finally degraded through proteosomes. Efficient autophagy or autophagocytosis is dependent on an equilibrium between the formation and elimination of autophagosomes; thus, a deficit in any part of this pathway will cause autophagic dysfunction. Autophagy plays a role in aging and agerelated diseases. Recent studies show that autophagy and changes in lysosomal activity are associated with both retinal aging and age-related macular degeneration. During autophagy, the cytosolic form of microtubule-associated protein 1A/1B- light chain 3, LC3-I is processed and recruited to the phagophore where it undergoes site specific proteolysis and lipidation near the C terminus to form LC3-II. Autophagy can be stimulated by a change of environmental conditions such as nutrient deprivation, various hormonal stimuli, and other factors.. Recent studies have shed light on the importance of autophagy in both normal development,tissue remodeling, and in pathological conditions. Autophagy does not only serve to protect cells, but it may also contribute to cell damage. Induction of autophagy serves as an early stress response in axonal dystrophy and may participate in the remodeling of axon structures. Autophagy also plays a major role in ocular patho-physiology. Morphological signs of autophagy have been described in the developing retina, participating in Eleutheroside-E programmed cell death. Molecular aging does occur in the trabecular meshwork, the main regulator of aqueous humor outflow. Oxidative damage in TM occur in primary open angle glaucomaand is strictly related with intraocular pressure increase and visual field damage. Salvianolic-acid-B Indeed, dysfunction of the TM increases the resistance of the outflow pathway and induces an increase in intraocular pressure. The number of TM cells decreases with agingthe histopathologic findings of primary open-angle glaucoma tissue being similar to those of aged tissue. Reactive oxygen speciesdamage TM cells, induce apoptosis, and promote cellular aging in this tissue. Oxidative damage and the associated mitochondrial dysfunction may result in energy depletion, accumulation of cytotoxic mediators and cell death. TM cells of the human eye have been suggested as the proper model system for the study of the cellular aging. It was reported that the number of TM cells decreases due to tissue damage induced by oxidative stressand senescence as occurring in glaucoma. Oxidative stress responses, including metabolites redistribution alter the acetylation status of proteins, in human cells with mitochondrial dysfunction and in aging. On the other hand, autophagy and mitophagy eliminate defective mitochondria and serve as a scavenger and apoptosis defender of cells in response to oxidative stress during aging. These scenarios mediate the adaptation of cells to respond to aging and age-related disorders for survival. In the natural course of aging, the homeostasis in the network of oxidative stress responses is disturbed by a progressive increase in the intracellular level of the ROS generated by defective mitochondria.