You will be provided with a reference and some statements. Please determine whether each statement is 'supported', 'unsupported', or 'unknown' with respect to the reference. Please note:
First, assess whether the reference contains any valid content. If the reference contains no valid information, such as a 'page not found' message, then all statements should be considered 'unknown'.
If the reference is valid, for a given statement: if the facts or data it contains can be found entirely or partially within the reference, it is considered 'supported' (data accepts rounding); if all facts and data in the statement cannot be found in the reference, it is considered 'unsupported'.

You should return the result in a JSON list format, where each item in the list contains the statement's index and the judgment result, for example:
[
    {
        "idx": 1,
        "result": "supported"
    },
    {
        "idx": 2,
        "result": "unsupported"
    }
]

Below are the reference and statements:
<reference>
1. Atherosclerosis. 2012 Aug;223(2):306-13. doi: 
10.1016/j.atherosclerosis.2012.06.013. Epub 2012 Jun 16.

Copper chelation by tetrathiomolybdate inhibits vascular inflammation and 
atherosclerotic lesion development in apolipoprotein E-deficient mice.

Wei H(1), Zhang WJ, McMillen TS, Leboeuf RC, Frei B.

Author information:
(1)Linus Pauling Institute and Department of Biochemistry & Biophysics, Oregon 
State University, Corvallis, OR 97331, USA.

Endothelial activation, which is characterized by upregulation of cellular 
adhesion molecules and pro-inflammatory chemokines and cytokines, and consequent 
monocyte recruitment to the arterial intima are etiologic factors in 
atherosclerosis. Redox-active transition metal ions, such as copper and iron, 
may play an important role in endothelial activation by stimulating 
redox-sensitive cell signaling pathways. We have shown previously that copper 
chelation by tetrathiomolybdate (TTM) inhibits LPS-induced acute inflammatory 
responses in vivo. Here, we investigated whether TTM can inhibit atherosclerotic 
lesion development in apolipoprotein E-deficient (apoE-/-) mice. We found that 
10-week treatment of apoE-/- mice with TTM (33-66 ppm in the diet) reduced serum 
levels of the copper-containing protein, ceruloplasmin, by 47%, and serum iron 
by 26%. Tissue levels of "bioavailable" copper, assessed by the 
copper-to-molybdenum ratio, decreased by 80% in aorta and heart, whereas iron 
levels of these tissues were not affected by TTM treatment. Furthermore, TTM 
significantly attenuated atherosclerotic lesion development in whole aorta by 
25% and descending aorta by 45% compared to non-TTM treated apoE-/- mice. This 
anti-atherogenic effect of TTM was accompanied by several anti-inflammatory 
effects, i.e., significantly decreased serum levels of soluble vascular cell and 
intercellular adhesion molecules (VCAM-1 and ICAM-1); reduced aortic gene 
expression of VCAM-1, ICAM-1, monocyte chemotactic protein-1, and 
pro-inflammatory cytokines; and significantly less aortic accumulation of M1 
type macrophages. In contrast, serum levels of oxidized LDL were not reduced by 
TTM. These data indicate that TTM inhibits atherosclerosis in apoE-/- mice by 
reducing bioavailable copper and vascular inflammation, not by altering iron 
homeostasis or reducing oxidative stress.

Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.

DOI: 10.1016/j.atherosclerosis.2012.06.013
PMCID: PMC3417757
PMID: 22770994 [Indexed for MEDLINE]
</reference>

<statements>
1. copper chelation reduced atherosclerotic lesion development by ~25% (whole aorta) to ~45% (descending aorta) in ApoE-deficient mice (Wei H et al., Atherosclerosis 2012;223:306–313), with reduced vascular inflammation
</statements>

Begin the assessment now. Output only the JSON list, without any conversational text or explanations.