Cardiovascular diseases (CVD) are the number one cause of death worldwide, with atherosclerosis, which is the formation of fatty plaques in the arteries, being the most common underlying cause. The activation of inflammatory events and endothelium dysfunction are crucial for the development and pathophysiology of atherosclerosis. Elevated circulating levels of low-density lipoprotein (LDL) have been associated with severity of atherosclerosis. LDL can undergo oxidative modifications, resulting in oxidised LDL (oxLDL). OxLDL has been found to have antigenic potential and contribute significantly to atherosclerosis-associated inflammation by activating innate and adaptive immunity. Various inflammatory stimuli such as interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-α) and intercellular adhesion molecule 1 (ICAM-1) play major roles in atherosclerosis. To date, studies have provided valuable insights into the role of oxLDL in the development of atherosclerosis. However, there remains a gap in understanding the specific pathways involved in this process. This review aims to provide and discuss the mechanisms by which oxLDL modulates signalling pathways that cause cardiovascular diseases by providing in vitro and in vivo experimental evidence. Its critical role in triggering and sustaining endothelial dysfunction highlights its potential as a therapeutic target. Advancing the understanding of its atherogenic role and associated signalling pathways could pave the way for novel targeted therapeutic strategies to combat atherosclerosis more effectively.