Ask your doctor if anything in here will change how they treat your plaque problems.
http://medicalxpress.com/news/2014-08-heart-disease.html
Scientists at the Interfaculty Institute of Biochemistry (IFIB) have
collaborated with colleagues from the Department of Pharmacy and the
Department of Dermatology of the University of Tübingen to identify a
long-overlooked function of vascular smooth muscle cells in
atherosclerosis.
Atherosclerosis, the buildup of plaques in the
arteries, leads to myocardial infarction and stroke and is the major
cause of death in the Western world. It is a chronic inflammatory
disease of the arteries arising from interactions of modified
lipoproteins and various cell types including monocyte-derived
macrophages from the blood and smooth muscle cells
(SMCs) in the vessel wall. "It is unclear, however, how each particular
cell type contributes to the development of an atherosclerotic lesion,"
says Professor Robert Feil, senior author of the study. "One highly
controversial issue is the contribution of vascular SMCs to plaque
growth."
The IFIB researchers performed lineage tracing experiments in mice,
in which they have genetically labeled mature SMCs in the vessel wall of
young mice before the onset of the disease and then monitored their
fate in older atherosclerotic animals. "Surprisingly, we found that SMCs
in the arterial wall can undergo clonal expansion during disease
progression and convert into macrophage-like cells
that have lost the classical SMC marker, α-smooth muscle actin," says
Dr. Susanne Feil, the first author of the publication. "It seems that
certain atherosclerotic lesions contain even more SMC-derived
macrophages than traditional monocyte-derived macrophages."
These findings indicate that previous studies based on immunostaining
of plaque cells for smooth muscle and macrophage markers have vastly
underestimated the role of SMCs and overestimated the role of
monocyte-derived macrophages in atherosclerosis. Robert Feil notes that
the results in the mouse model might also translate to humans.
"Targeting SMC-to-macrophage transdifferentiation could be a novel
therapeutic strategy to treat atherosclerotic heart disease and perhaps
many other diseases with a smooth muscle component."
This work was supported by grants from VolkswagenStiftung, Deutsche
Forschungsgemeinschaft, fortüne-Programm der Medizinischen Fakultät der
Universität Tübingen, and Dr. Karl Kuhn-Stiftung.
Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 29,112 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke.DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER, BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.
No comments:
Post a Comment