Editing Atherosclerosis (section)

===Lipids===
An indication of the role of [[high-density lipoprotein]] (HDL) on atherosclerosis has been with the rare [[ApoA-1 Milano|Apo-A1 Milano]] human genetic variant of this [[High-density lipoprotein|HDL]] protein. A small short-term trial using bacterial synthesized human [[ApoA-1 Milano|Apo-A1 Milano]] HDL in people with unstable angina produced a fairly dramatic reduction in measured coronary plaque volume in only six weeks vs. the usual increase in plaque volume in those randomized to placebo. The trial was published in ''[[JAMA]]'' in early 2006.{{Citation needed|date=February 2018}}  Ongoing work starting in the 1990s may lead to human clinical trials—probably by about 2008.{{update inline|date=June 2014}}  These may use synthesized Apo-A1 Milano HDL directly, or they may use gene-transfer methods to pass the ability to synthesize the Apo-A1 Milano HDLipoprotein.{{Citation needed|date=February 2018}}

Methods to increase HDL particle concentrations, which in some animal studies largely reverses and removes atheromas, are being developed and researched.{{Citation needed|date=February 2018}} However, increasing HDL by any means is not necessarily helpful. For example, the drug [[torcetrapib]] is the most effective agent currently known for raising HDL (by up to 60%). However, in clinical trials, it also raised deaths by 60%.  All studies regarding this drug were halted in December 2006.<ref>{{cite journal | vauthors = Barter PJ, Caulfield M, Eriksson M, Grundy SM, Kastelein JJ, Komajda M, Lopez-Sendon J, Mosca L, Tardif JC, Waters DD, Shear CL, Revkin JH, Buhr KA, Fisher MR, Tall AR, Brewer B | title = Effects of torcetrapib in patients at high risk for coronary events | journal = The New England Journal of Medicine | volume = 357 | issue = 21 | pages = 2109–2122 | date = November 2007 | pmid = 17984165 | doi = 10.1056/NEJMoa0706628 | doi-access = free }}</ref>

The actions of [[macrophage]]s drive atherosclerotic plaque progression.
''Immunomodulation of atherosclerosis'' is the term for techniques that modulate immune system function to suppress this macrophage action.<ref name=Nilsson>{{cite journal | vauthors = Nilsson J, Hansson GK, Shah PK | title = Immunomodulation of atherosclerosis: implications for vaccine development | journal = Arteriosclerosis, Thrombosis, and Vascular Biology | volume = 25 | issue = 1 | pages = 18–28 | date = January 2005 | pmid = 15514204 | doi = 10.1161/01.ATV.0000149142.42590.a2 | doi-access = free }}</ref>

Involvement of [[lipid peroxidation]] chain reaction in atherogenesis<ref>{{cite journal | vauthors = Spiteller G | title = The relation of lipid peroxidation processes with atherogenesis: a new theory on atherogenesis | journal = Molecular Nutrition & Food Research | volume = 49 | issue = 11 | pages = 999–1013 | date = November 2005 | pmid = 16270286 | doi = 10.1002/mnfr.200500055 }}</ref> triggered research on the protective role of the heavy isotope ([[Deuterated drug|deuterated]]) [[polyunsaturated fatty acid]]s (D-PUFAs) that are less prone to oxidation than ordinary PUFAs (H-PUFAs). PUFAs are [[essential nutrients]] – they are involved in metabolism in that very form as they are consumed with food. In [[transgenic mice]], a model for human-like lipoprotein metabolism, adding D-PUFAs to the diet reduced body weight gain, improved cholesterol handling, and reduced atherosclerotic damage to the aorta.<ref>{{cite journal | vauthors = Berbée JF, Mol IM, Milne GL, Pollock E, Hoeke G, Lütjohann D, Monaco C, Rensen PC, van der Ploeg LH, Shchepinov MS | title = Deuterium-reinforced polyunsaturated fatty acids protect against atherosclerosis by lowering lipid peroxidation and hypercholesterolemia | journal = Atherosclerosis | volume = 264 | pages = 100–107 | date = September 2017 | pmid = 28655430 | doi = 10.1016/j.atherosclerosis.2017.06.916 }}</ref><ref>{{cite journal | vauthors = Tsikas D | title = Combating atherosclerosis with heavy PUFAs: Deuteron not proton is the first | journal = Atherosclerosis | volume = 264 | pages = 79–82 | date = September 2017 | pmid = 28756876 | doi = 10.1016/j.atherosclerosis.2017.07.018 }}</ref>