Endoplasmic reticulum (ER) stress is a key factor linking inflammation and obesity-associated adipose tissue dysfunction. Obesity is a chronic disease characterized by low-grade inflammation, which disrupts normal metabolic functions and is closely associated with ER stress. ER stress activates the unfolded protein response (UPR), which includes three main branches: PERK, IRE1, and ATF6. These pathways regulate protein folding, lipid metabolism, and inflammation, playing a crucial role in obesity-related metabolic disorders. ER stress can lead to the production of reactive oxygen species, disrupt energy metabolism, and promote oxidative stress and inflammation. In obese individuals, ER stress is significantly elevated in adipose tissue, contributing to the activation of inflammatory pathways such as JNK, IKK, and NF-κB. The UPR pathway also plays a role in the development of metabolic inflammation, which is a key feature of obesity. Targeting ER stress may offer a potential therapeutic approach for obesity and its associated diseases, including type 2 diabetes and metabolic syndrome. The review discusses the mechanisms by which ER stress affects adipose tissue function and inflammation in obesity, highlighting the importance of understanding ER homeostasis and the potential therapeutic role of ER stress in obesity. The study also explores the interaction between adipose tissue function and ER stress, emphasizing the role of adipokines and inflammatory pathways in obesity. The review concludes that targeting ER stress represents a promising therapeutic strategy for treating obesity and its complications.Endoplasmic reticulum (ER) stress is a key factor linking inflammation and obesity-associated adipose tissue dysfunction. Obesity is a chronic disease characterized by low-grade inflammation, which disrupts normal metabolic functions and is closely associated with ER stress. ER stress activates the unfolded protein response (UPR), which includes three main branches: PERK, IRE1, and ATF6. These pathways regulate protein folding, lipid metabolism, and inflammation, playing a crucial role in obesity-related metabolic disorders. ER stress can lead to the production of reactive oxygen species, disrupt energy metabolism, and promote oxidative stress and inflammation. In obese individuals, ER stress is significantly elevated in adipose tissue, contributing to the activation of inflammatory pathways such as JNK, IKK, and NF-κB. The UPR pathway also plays a role in the development of metabolic inflammation, which is a key feature of obesity. Targeting ER stress may offer a potential therapeutic approach for obesity and its associated diseases, including type 2 diabetes and metabolic syndrome. The review discusses the mechanisms by which ER stress affects adipose tissue function and inflammation in obesity, highlighting the importance of understanding ER homeostasis and the potential therapeutic role of ER stress in obesity. The study also explores the interaction between adipose tissue function and ER stress, emphasizing the role of adipokines and inflammatory pathways in obesity. The review concludes that targeting ER stress represents a promising therapeutic strategy for treating obesity and its complications.