Endoplasmic reticulum (ER) is the predominant membrane structure in eukaryotic cells and is a key organelle for the occurrence of important intracellular physiological processes. Under the action of various internal and external factors, the homeostasis of ER is disrupted to block protein processing and transport, and the accumulation of unfolded or misfolded proteins in the ER lumen, forms endoplasmic reticulum stress (ERS) and triggers the unfolded protein response (UPR). Moderate ERS reduces protein synthesis, promotes protein degradation, and increases molecular chaperones that assist protein folding through the UPR signaling pathway, ultimately relieving ER stress. However, if the ERS is too strong or prolonged and exceeds the cell's ability to regulate itself, the UPR can initiate apoptosis and lead to diseases.Numerous studies have shown that ERS is closely associated with the development of several cardiovascular diseases (CVD). This review focuses on the research progress of UPR in several common types of CVD and targets UPR as a potential therapeutic approach for CVD.