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Atherosclerosis & Cholesterol

27 important questions on Atherosclerosis & Cholesterol

What are the riskfactors for atherosclerosis?

High cholesterol (LDL), low HDL, hypertension, diabetes.

Why does atherosclerosis not happen in veins?

Atherosclerosis only happens in arteries as veins lack the strong pulse and have a different structure.

How is atherosclerosis treated?

With angioplasty and stents (bare-metal or drug-eluting).
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What is in-stent restenosis?

In in-stent restenosis there is excessive SMC proliferation within the stent.

How is in-stent restenosis treated? And what are the risks of this treatment?

With drug-eluting stents.
- Rapamycin/Sirolimus: mTOR enhanced expression of p27
- Taxol/ Paclitaxel: microtubule disruption

However, both drugs inhibit growth of all cells (both SMC and EC growth). Therefore there is no endothelial recovery increasing the risk for thrombosis. Double anti-platelet therapy however leads to an increased risk for bleeding at other surgeries.

What is Nur77 and what is its role in atherosclerosis?

Nur 77 is a nuclear receptor (transcription factor).
- Inhibits SMC growth
- Promotes EC survival
- Reduces inflammatory response macrophages

Which SNP is important in in-stent restenosis?

P27kip1 . P27 inhibits the SMC growth.

How can SNPs be applications in the clinic?

They can help with the  identification of patients with an increased risk of in-stent restenosis.

" use the right stent for the right patient".

How does atherosclerosis develop?

Excessive LDL --> oxidation forms oxLDL --> particles activate endothelial cells --> monocytes migrate into the tissue --> macrophages scavenge oxLDL --> macrophages become big foam cells --> macrophages cannot go back into circulation --> produce cytokines and growthfactors --> more monocyte migration.

* oxLDL is not recognized by LDLR  
* smoking leads to a lot ROS induction --> more oxLDL

What are the genetic components of atherosclerosis?

- Familiar Hypercholesterolemia (FH): mutation LDL receptor
- Tangier dieseas: mutation ABCA1
- Genetic predisposition (good & bad SNPs)

What is an Abdominal Aortic Aneurysm (AAA)?

It is the dilation of the aorta which results in decreased vessel wall integrity, eventually leading to aortic rupture. Structural proteins of the vessel wall, like the elastic laminae and fibrillar collagens, are degraded and in the end unstable to withstand the aortic pressure.

* AAA form later in life and are less symptomatic compared to atherosclerosis.

When is an AAA eligible for surgery?

The AAA is eligible for surgery when it is larger than 5.5 cm (normal aorta is 2-3 cm).

How much does an AAA grow every year?

0.3 cm/year (0.4 cm/year in smokers).

By what is the growth of the AAA caused?

AAA growth is caused by extracellular matrix degradation, involving proteases produced by inflammatory cells.

What are the risk factors of an aneurysm?

Age (>50), Gender (M), Blood pressure, Smoking, Family history, atherosclerosis

What is the most affected in atherosclerosis? And in Aneurysms?

- Atherosclerosis: intima (endothelial cells)
- Aneurysms: Adventia (fibroblasts) and Media (smooth muscle cells)

How doe endothelial cells sense and react t mechanic stress?

Cilia sense mechanic stress --> eNOS activation --> NO generation --> SMC vasodilation.

How does smoking cause endothelial dysfunction?

Smoking induces eNOS uncoupling. The vessel cannot relax/vasodialate when mechanic stress is present.

What happens to the adventia in aneurysms?

Normally, the adventia (fibroblasts) limits the expansion. However, the adventia is degraded in aneurysms and therefore the vessel wall becomes rupture prone.

How can aneurysms be prevented? And what are the risks of these drugs?

- Anti-inflammatory drugs: stops inflammatory cells and therefore the production of proteases.
* most anti-inflammatory drugs inhibit proliferation/migration of SMC, repair declines.

- Doxycyclin: inhibits proteases and therefore degradation of aorta. 
* Is anti-bacteria, but also inhibits mitochondria function. (macrophages, T-cells, SMCs).

What is the effect of an dominant-active variant of a nuclear receptor in a cell in which the 'normal' nuclear receptor is already present?

The nuclear receptor will always be active, so the pathway it controls will always be on. Nuclear receptors change gene expression profiles, so those will also change.

How can a slow-growing atherosclerotic lesion lead to an acute myocardial infarction?

The arteries are slowly narrowing. Once a plaque rupture happens a blood cloth can be formed which can block the artery.

The SMC normally help to stabilize the clot.

How do LXRs (Liver X Receptors) control the cellular cholesterol?

LXRs are ligand dependent transcription factors that belong to the nuclear receptor family. Their ligands are  oxidized cholesterol metabolites and intermediates of the cholesterol biosynthetic pathway (both increase when cellular cholesterol levels rise). LXRs induce the expression of genes whose main function is to reduce the cellular cholesterol burden (ABCA1/ABCG1).  LXRs also limit cholesterol uptake via LDLR pathway, which is dependent on the transcriptional regulation of the E3-ubiquitin ligase IDOL. 

* LXRs are normally inhibited
* Always in the nucleus

How do SREBPs control cellular cholesterol?

When the cholesterol levels in the ER membrane decline, SCAP-bound SREBPs travel to the Golgi where they are cleaved and able to travel to the nucleus to bind the their promotor. They induce the enzymes required for de novo cholesterol synthesis via the mevalonate pathway. SREBPs also induce expression of the LDLR resulting in increased uptake of exogenous LDL-cholesterol.

Transcription factor = SREPB2
Sensor = SCAP
Inhibitor= INSIG    

* Er membrane = 5% cholesterol (SCAP is sensor)

How does uRNA33a regulate the efflux of cholesterol?

The activation of SREBP results in more uRNA33a which results in less ABCA1. Therefore there is less cholesterol efflux and the cellular cholesterol level rises. However, the rise in cellular cholesterol inhibits SREBP.

How does the cholesterol-dependent degradation of squalence go?

SM converts squalance into MOS which is then converted into cholesterol (squalance is the precursor of cholesterol). However, MARCH6 ubiquitinates SM after which it is degraded. So no more cholesterol is formed.
Cholesterol inhibits MARCH6.

How does the degradation of LDLR by IDOL go?

LDLR stimulates the cholesterol uptake, which activates LXR. LXR activates IDOL which ubiquitinates LDLR, so the uptake goes down.

IDOL = E3-ligase inducabel degrader LDL receptor (ubiquitinates LDLR)

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The question on the page originate from the summary of the following study material:

Medical Biochemistry and Pathophysiology

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