What is it about?
The answer is "No, BUT." Major changes in the last few years show that cancer is a result of expansion of clones of cells. Clonality , however, turns out to be part of the way many tissues develop including the immune system hair follicles, and possibly even the brain. We also know that the atheroscoerotic lesion is a clone ... probably a result of normal processes in the development or response to injury of human arteries. So, if we understand how clonality of arterial wall cells leads to atherosclerosis, we may be able to prevent the disease or ameliorate its consequences.
Featured Image
Why is it important?
This is a review article that discuss the molecular genetics that underlie clonality in the artery wall. The article suggests strategies to understand how the atheroscleritic clones arise.
Perspectives
It is now fifty years since my mentor, Earl Benditt, discovered the clonality of atherosclerosis. His work was attacked by many because of the research community's focus of lipids. That focus was hugely important but resulted in a lack of effort to understand the simple fact that the lesions liley would never occur if clonal expansion did not exist. Today, lipid lowering therapies do prolong life but the ultimate clinical events remain largely poorly understood. Partof that answer likely lies in understanding Benditt;s work.
Stephen Schwartz
Read the Original
This page is a summary of: An update on clonality: what smooth muscle cell type makes up the atherosclerotic plaque?, F1000Research, December 2018, Faculty of 1000, Ltd.,
DOI: 10.12688/f1000research.15994.1.
You can read the full text:
Contributors
The following have contributed to this page
