|
Lipoprotein(a)
-
維基百科
：
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.
Lp(a) is assembled at
the hepatocyte cell membrane surface, while other
scenarios exist with regard to the location of
assembly. It mainly exists in plasma. Lp(a) contributes
to the process of atherogenesis. Because of its
structural similarity to plasminogen and tissue
plasminogen activator, competitive inhibition leads to
reduced fibrinolysis, and as a result of the stimulation
of secretion of plasminogen activator inhibitor 1, Lp(a)
leads to thrombogenesis. It may also enhance coagulation
by inhibiting the function of tissue factor pathway
inhibitor. Lp(a) carries cholesterol and binds
atherogenic proinflammatory oxidized phospholipids as a
preferential carrier of oxidized phospholipids in human
plasma, which attract inflammatory cells to vessel walls
and leads to smooth muscle cell proliferation. Moreover,
Lp(a) is also hypothesized to be involved in wound
healing and tissue repair, interacting with components
of the vascular wall and extra cellular matrix.
Apo(a), a distinct feature of the Lp(a)
particle, binds to immobilized fibronectin and endows
Lp(a) with the serine-proteinase-type proteolytic
activity.
However, individuals
without Lp(a) or with very low Lp(a) levels seem to be
healthy. 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 that adopted diets less abundant
in vitamin C may have used Lp(a) as an ascorbic-acid
surrogate to repair arterial walls.
-
編者補充：LDL+Apo(a)=Lp(a)，Apo(a)是一種黏性蛋白，可以黏住纖維蛋白(Fibrin)，讓纖溶酶原無法與纖維蛋白結合，無法行使纖溶酶原(plasminogen)分解凝固血塊的作用。所以含有Apo(a)的Lp(a)就成為很有效的結締組織修復原料，這也是所有脂質蛋白裡面最特別的顆粒。
-
Apo(a)的分子結構裡面有黏性蛋白特有的胺基酸排序(精氨酸-甘胺酸-天冬胺酸)，所以Apo(a)也具有黏性。
-
Apo(a)不全然是不好的，它也有它的好處：
1.Apo(a)的黏性可以穩固細胞外的基質(extracellular matrix)。
2.Apo(a)能與血液凝固系統相互作用。
3.Apo(a)具有抗氧化劑的防護功能。
4.Apo(a)能抑制plasmin誘發的蛋白質分解作用。
5.Apo(a)參與了一些發育過程，例如˙：細胞分化、外型的生成、受孕、智力發展。
-02.jpg)
-pro-atherogenesis.jpg)
|
+or+Lp(a).jpg)
-03.jpg)
