https://en.wikipedia.org/wiki/Lipoprotein(a)#Function
Lipoprotein(a) (also called Lp(a) or LPA) is a lipoprotein subclass. Genetic studies and numerous epidemiologic studies have identified Lp(a) as a risk factor for atherosclerotic diseases such as coronary heart disease and stroke.[3][4][5][6][7]
Lipoprotein(a) was discovered in 1963 by Kåre Berg.[8] The human gene encoding apolipoprotein(a) was cloned in 1987.[9]
Lipoprotein(a) was discovered in 1963 by Kåre Berg.[8] The human gene encoding apolipoprotein(a) was cloned in 1987.[9]
Contents
- 1 Structure
- 2 Catabolism and clearance
- 3 Populations
- 4 Function
- 5 Pathology
- 6 Lipoprotein(a) and disease
- 7 Diagnostic testing
- 8 Treatment
- 9 Interactions
- 10 See also
- 11 References
- 12 Further reading
- 13 External links
Nonetheless, individuals without Lp(a) or with very low Lp(a) levels seem to be healthy.[31] Thus, plasma Lp(a) is not vital, at least under normal environmental conditions. Since apo(a)/Lp(a) derived rather recently in mammalian evolution - only old world monkeys and humans have been shown to harbour Lp(a) - its function might not be vital, but just evolutionarily advantageous under certain environmental conditions, e.g. in case of exposure to certain infectious diseases.
Another possibility, suggested by Linus Pauling, is that Lp(a) is a primate adaptation to L-gulonolactone oxidase (GULO) deficiency, found only in certain lines of mammals. GULO is required for converting glucose to ascorbic acid (vitamin C), which is needed to repair arteries; following the loss of GULO, those primates who adopted diets less abundant in vitamin C may have used Lp(a) as an ascorbic-acid surrogate to repair arterial walls.[32]
Another possibility, suggested by Linus Pauling, is that Lp(a) is a primate adaptation to L-gulonolactone oxidase (GULO) deficiency, found only in certain lines of mammals. GULO is required for converting glucose to ascorbic acid (vitamin C), which is needed to repair arteries; following the loss of GULO, those primates who adopted diets less abundant in vitamin C may have used Lp(a) as an ascorbic-acid surrogate to repair arterial walls.[32]
Lp(a) carries cholesterol and binds atherogenic proinflammatory oxidized phospholipids as a preferential carrier of oxidized phospholipids in human plasma,[25] which attract inflammatory cells to vessel walls and leads to smooth muscle cell proliferation.[26] Moreover, Lp(a) also is hypothesized to be involved in wound healing and tissue repair, interacting with components of the vascular wall and extra cellular matrix.[27][28][29]
