Atherosclerosis, a persistent inflammatory condition affecting the arteries, continues to be a major contributor to cardiovascular death globally despite improvements in its treatment. Conventional risk factors such as elevated cholesterol levels, diabetes, and smoking cannot completely account for all instances, emphasizing the need to identify novel treatment targets. Lipoprotein(a) [Lp(a)] is a type of lipoprotein particle that is similar in structure to low-density lipoprotein (LDL-C) but different because it contains apolipoprotein(a) [apo(a)]. Genetic factors, particularly the LPA gene, predominantly determine Lp(a) levels, which vary significantly across populations. Cardiovascular disease (CVD) is strongly associated with high Lp(a) levels. However, researchers are still investigating the precise mechanisms by which Lp(a) contributes to the development of arterial diseases. The metabolism of Lp(a) is complex and includes its synthesis in the liver, its combination with apolipoprotein B-₁₀₀ (apo-B₁₀₀), and its interactions with several receptors for its removal, particularly from the liver and kidneys. In addition to its involvement in atherosclerosis, Lp(a) may also serve physiological purposes such as contributing to wound healing and angiogenesis. Factors that affect Lp(a) levels include genetic composition, acute-phase reactions, and hormonal fluctuations. Despite extensive investigations, the relationship between physical activity and Lp(a) levels remains unclear. This review presents an up-to-date thorough examination of Lp(a) metabolism, pathogenesis, and possible therapeutic approaches.