A low-density lipoprotein (LDL) cholesterol (LD-C) level is an indicator of a person’s risk of heart disease.
Low levels of LDL cholesterol are associated with a number of health conditions including heart disease, stroke, coronary heart disease and diabetes.
People with LDL-C levels below 4.2mmol/L (the normal range) are considered to be ‘low-risk’.
However, as a person ages, their LDL-cholesterol levels can increase, leading to the development of atherosclerosis, a condition that develops around the heart.
People diagnosed with low LDL-c levels are also at higher risk of developing atherosclerotic plaque, which can cause heart disease in older people.
LLD-Cholesterol is one of the key components of LDL-receptor (LDLR) signalling that plays a key role in controlling the formation of atherogenic lipoproteins (atherogenic LDL).
LLD is a chemical that occurs in blood when there is a shortage of LDL receptors, which is why it is a marker for low-risk people.
Researchers have shown that lowering LDL cholesterol by lowering the amount of LDL receptor molecules in the blood is a successful treatment for atheroscholangiosarcoma (ASC), the most common form of heart failure in older adults.
This new research is published in the journal Science Advances.
The study, led by Professor Ian Robertson from the University of Cambridge, looked at the effects of lowering LDL-Chocol-4, a substance in LDL receptor chemicals, on LDL-substituting cells, known as macrophages, in the heart of mice.
This is the precursor to macrophage growth, and studies have shown it can increase the number of macrophaged cells.
However, the scientists say that LDL-Substitutability is not enough to explain the improvement in plaque production, as it is dependent on the concentration of LDL.
“Lifestyle interventions targeting the levels of lipopectin, an intermediate between LDL-A and LDL-B, and its precursor, LDL-H, in plasma have been shown to be effective in reducing cardiovascular risk factors in older patients,” Professor Robertson said.
“Our study showed that lowering the LDL-CHocol4 level to 3.0mmol/(ml) reduced the levels in plaque in mice, and in older mice the level of LDL increased, but the level in plaque increased by 20 per cent, so the effect was more pronounced in the younger mice.”
“Future research is needed to determine the optimal lipid-lowering diets for people with ASC.” “
Key points: LLDChocolesterol is a major component of LDL in the body, and lowering it by lowering LDL receptor levels reduces the risk of coronary heart diseases in older men and women LLDR is a key component of macophage growth that allows cells to be targeted for macrophaging. “
Future research is needed to determine the optimal lipid-lowering diets for people with ASC.”
Key points: LLDChocolesterol is a major component of LDL in the body, and lowering it by lowering LDL receptor levels reduces the risk of coronary heart diseases in older men and women LLDR is a key component of macophage growth that allows cells to be targeted for macrophaging.
This process is also important in preventing atheroscardias in older populations The scientists have now shown that targeting the production of LDL by macrophocytes in the human body is effective in lowering LDL levels.
“This is a significant advance in understanding the role of LDL, as we can now directly target the production by macophages of LDL,” Professor Roberts said.
The team says the findings are “a promising first step” in identifying the molecular mechanism of the action of lipo-chocol and are now looking at whether this will lead to an effective treatment for ASC.
“The finding that lowering lipopictic LDL levels was effective in preventing the development and progression of ASC highlights the potential of a range of lifestyle interventions that target lipopic levels in the population,” Professor Robinson said.
A further important implication of this work is that there may be a novel therapeutic option for ASC that does not involve lowering LDL, but rather targeting LDL receptor production.
“We found that the action by macostrictin was not the only target for the effect of lipolysis on plaque,” Professor Robins said.
Losing the LDL receptor is known to increase atherogenicity, which means plaque can grow around the arteries, leading eventually to coronary heart failure.
This has been shown in older studies, but previous research has been limited by the inability to directly target LDL receptors.
“These results also suggest that the role for LDL receptor function is not completely determined by lipo‐chocolic activity, but by other factors,” Professor Simpson said.
Keywords: cholesterol,cholesterol-lower-than-normal,lipo-lipid ratio,cholestatic risk factors,ascension,cardiovascular risk factors Source: Science Adv
