ISSN: 2578-4811
Authors: Maher M. Akl* and Amr Ahmed
This letter explores the intricate relationship between endoplasmic reticulum (ER) stress and its effects on cellular environment, specifically focusing on anaerobic respiration and its role in tumor activity and the pre-glucolipotoxicity stage. ER stress disrupts protein homeostasis, leading to the accumulation of misfolded proteins within the ER [1]. To restore proteostasis, cells activate an adaptive unfolded protein response involving various signaling pathways. However, ER stress extends beyond protein processing and transcription, exerting epigenetic effects [2]. Immune responses occurring during cellular stresses often rely on the unfolded protein response to maintain ER homeostasis. Dysregulated ER stress responses can contribute to the development of autoimmune disorders, making the unfolded protein response a potential therapeutic target [3]. Additionally, ER stress alters cellular metabolism, shifting energy utilization from aerobic to anaerobic pathways, such as fermentation [4]. This metabolic adaptation enables cells to meet energy demands under stressful conditions. Notably, ER stress also impacts the activity of the P53 protein, a critical regulator of cell growth and tumor suppression. Inhibition of P53 alters gene expression, favoring the development of tumor-promoting genes. Hence, understanding the complex interplay between ER stress and cellular processes provides insights into tumor growth regulation [5].
Keywords: Cell Growth; Tumor; Type 2 Diabetes Mellitus; Adipocytes; Glucolipotoxicity; ER Stress
