IntroductionStress is a problem faced by all organisms in nature. It is a natural part of life as a response to stimuli. Over the years it has developed different connotations, but stress is defined as the organism's non-specific response to any request for change” (Selye, 1998). Therefore, cells also experience stress. In some circumstances, short-term stress can be beneficial to the cell; however, prolonged stress (especially in the endoplasmic reticulum [ER]) created by harmful stimuli such as heat, shock, oxidation, viruses, or other factors can lead to an overabundance of unfolded proteins (Szegezdi, 2007). Prolonged ER stress will therefore lead to pathological conditions and even the induction of apoptosis (orchestrated cell death) (Lai, Teodoro, & Volchuk, 2007). Since the ER is the organelle that monitors the correct folding and release of proteins, when stressed, a recovery response from the cell is required, otherwise disease and/or cell death will surely follow (Kostova & Wolf, 2003). stress, one of the first responses to stress is carried out by the renal proximal tubular cells (kidney). This reaction consists of activating the unfolded protein response (UPR), during which the cell: (a) stops protein synthesis, (b) recovers essential proteins and messenger ribonucleic acid (RNA), and (c ) degrades and/or folds proteins necessary for daily processes in an attempt to maintain the cell's internal homeostasis (Fukasawa, 2012). If the UPR and proteasomes fail to stabilize the cell, autophagy (degradation of autocells) may occur as a last ditch effort to preserve cellular homeostasis and prolong cellular life (Benbrook & Long, 2012). Consequently, ER stress and the cellular response to it can have profound effects on the human body. A clear example, the subject of study in this research, is a disease that afflicts approximately 30% of all diabetics and is one of the main causes in the development of end-stage renal disease (National Kidney Foundation, 2012). This serious disease is diabetic nephropathy (DN). Several processes, including genetic, environmental, behavioral, and cellular factors, contribute to the development of diabetes. The onset of DN is believed to result from excessive amounts of sugar that are retained in the blood and are then filtered into the urine and absorbed by the kidneys. These unusually high and prolonged levels of urine and blood sugar levels create cellular stress, including ER stress, and produce body-wide high levels of glucose and/or protein in the urine (National Institute of Diabetes and Digestive Diseases and Kidneys), 2012).