-
- Clinton S Robbins, Ingo Hilgendorf, Georg F Weber, Igor Theurl, Yoshiko Iwamoto, Jose-Luiz Figueiredo, Rostic Gorbatov, Galina K Sukhova, Louisa M S Gerhardt, David Smyth, Caleb C J Zavitz, Eric A Shikatani, Michael Parsons, Nico van Rooijen, Herbert Y Lin, Mansoor Husain, Peter Libby, Matthias Nahrendorf, Ralph Weissleder, and Filip K Swirski.
- 1] Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA. [2] Toronto General Research Institute, University Health Network, Toronto, Ontario, Canada. [3] Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada. [4] Department of Immunology, University of Toronto, Toronto, Ontario, Canada. [5].
- Nat. Med. 2013 Sep 1;19(9):1166-72.
AbstractDuring the inflammatory response that drives atherogenesis, macrophages accumulate progressively in the expanding arterial wall. The observation that circulating monocytes give rise to lesional macrophages has reinforced the concept that monocyte infiltration dictates macrophage buildup. Recent work has indicated, however, that macrophage accumulation does not depend on monocyte recruitment in some inflammatory contexts. We therefore revisited the mechanism underlying macrophage accumulation in atherosclerosis. In murine atherosclerotic lesions, we found that macrophages turn over rapidly, after 4 weeks. Replenishment of macrophages in these experimental atheromata depends predominantly on local macrophage proliferation rather than monocyte influx. The microenvironment orchestrates macrophage proliferation through the involvement of scavenger receptor A (SR-A). Our study reveals macrophage proliferation as a key event in atherosclerosis and identifies macrophage self-renewal as a therapeutic target for cardiovascular disease.
Notes
Knowledge, pearl, summary or comment to share?You can also include formatting, links, images and footnotes in your notes
- Simple formatting can be added to notes, such as
*italics*
,_underline_
or**bold**
. - Superscript can be denoted by
<sup>text</sup>
and subscript<sub>text</sub>
. - Numbered or bulleted lists can be created using either numbered lines
1. 2. 3.
, hyphens-
or asterisks*
. - Links can be included with:
[my link to pubmed](http://pubmed.com)
- Images can be included with:
![alt text](https://bestmedicaljournal.com/study_graph.jpg "Image Title Text")
- For footnotes use
[^1](This is a footnote.)
inline. - Or use an inline reference
[^1]
to refer to a longer footnote elseweher in the document[^1]: This is a long footnote.
.