Targeting the Role of Lipoprotein (a) in Stroke.

Stroke is the third leading cause of death in the United States, behind only heart disease and cancer, with over 140,000 associated deaths per year.

Considerable research is ongoing to examine the role of modifiable risk factors which may cause or contribute to stroke. Although age and family history are generally considered to be the major risk factors, there are several modifiable and non-modifiable risk factors that are linked to the pathogenesis of a stroke. Lipoprotein (a), or Lp(a), is a type of low-density lipoprotein containing an integral apolipoprotein B100 (apoB100) component with an attached apolipoprotein A-1 (ApoA-1) isoform via a disulfide linkage. Lp(a) metabolism is of great interest as it sheds light on its role in pathogenesis of not only cardiovascular disorders but also stroke. Although Lp(a) has been identified as an "LDL-like particle", its metabolism differs from low density lipoprotein (LDL). Despite some ambiguity in the literature regarding the causative effect of Lp(a) on stroke, there are clear associations of high plasma Lp(a) concentration and risk of stroke. Furthermore, the small isoforms of ApoA-1-containing lipoproteins have been shown to increase atherogenicity in atherosclerotic patients.

Currently, there is little research examining the importance of small molecule Lp(a) distribution and risk for stroke, both on a first-case and recurrent basis. Understanding the role of Lp (a) in stroke requires investigating its molecular mechanisms particularly the key microRNA (s) components that control its expression and function (s). Therefore, the main objective of this review is to discuss the broader link between Lp(a) and stroke and to identify opportunities for future investigation and potential research prospects on the role of Lp (a) in stroke.