Deficiency of endogenous acute phase serum amyloid A does not affect atherosclerotic lesions in apolipoprotein E-deficient mice.

Deficiency of endogenous acute phase serum amyloid A does not affect atherosclerotic lesions in apolipoprotein E-deficient mice.

[Anonymous].  2014.  Deficiency of endogenous acute phase serum amyloid A does not affect atherosclerotic lesions in apolipoprotein E-deficient mice.. Arteriosclerosis, thrombosis, and vascular biology. 34(2):255-61.

Increased atherosclerosis in mice with increased vascular biglycan content.

Biglycan deficiency: increased aortic aneurysm formation and lack of atheroprotection.

A brief elevation of serum amyloid A is sufficient to increase atherosclerosis.

Prevention of renal apoB retention is protective against diabetic nephropathy: role of TGF-β inhibition.

Serum amyloid A3 is pro-atherogenic.

Elevated circulating TGF-β is not the cause of increased atherosclerosis development in biglycan deficient mice.

Serum Amyloid A Is an Exchangeable Apolipoprotein.

Coordinated post-transcriptional regulation of Hsp70.3 gene expression by microRNA and alternative polyadenylation.

Myeloid-specific IκB kinase β deficiency decreases atherosclerosis in low-density lipoprotein receptor-deficient mice.