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@ARTICLE{Ebert:163653,
author = {Ebert, Max L A and Schmidt, Vanessa F and Pfaff, Lena and
von Thaden, Anne and Kimm, Melanie A and Wildgruber, Moritz},
title = {{A}nimal {M}odels of {N}eointimal {H}yperplasia and
{R}estenosis: {S}pecies-{S}pecific {D}ifferences and
{I}mplications for {T}ranslational {R}esearch.},
journal = {JACC Basic to translational science},
volume = {6},
number = {11},
issn = {2452-302X},
address = {Washington, DC},
publisher = {American College of Cardiology},
reportid = {DZNE-2022-00399},
pages = {900 - 917},
year = {2021},
abstract = {The process of restenosis is based on the interplay of
various mechanical and biological processes triggered by
angioplasty-induced vascular trauma. Early arterial recoil,
negative vascular remodeling, and neointimal formation
therefore limit the long-term patency of interventional
recanalization procedures. The most serious of these
processes is neointimal hyperplasia, which can be traced
back to 4 main mechanisms: endothelial damage and
activation; monocyte accumulation in the subintimal space;
fibroblast migration; and the transformation of vascular
smooth muscle cells. A wide variety of animal models exists
to investigate the underlying pathophysiology. Although
mouse models, with their ease of genetic manipulation,
enable cell- and molecular-focused fundamental research, and
rats provide the opportunity to use stent and balloon models
with high throughput, both rodents lack a lipid metabolism
comparable to humans. Rabbits instead build a bridge to
close the gap between basic and clinical research due to
their human-like lipid metabolism, as well as their size
being accessible for clinical angioplasty procedures. Every
different combination of animal, dietary, and injury model
has various advantages and disadvantages, and the decision
for a proper model requires awareness of species-specific
biological properties reaching from vessel morphology to
distinct cellular and molecular features.},
subtyp = {Review Article},
keywords = {Apo, apolipoprotein (Other) / CETP, cholesteryl ester
transferase protein (Other) / ECM, extracellular matrix
(Other) / FGF, fibroblast growth factor (Other) / HDL,
high-density lipoprotein (Other) / LDL, low-density
lipoprotein (Other) / LDLr, LDL receptor (Other) / PDGF,
platelet-derived growth factor (Other) / TGF, transforming
growth factor (Other) / VLDL, very low-density lipoprotein
(Other) / VSMC, vascular smooth muscle cell (Other) /
angioplasty (Other) / animal model (Other) / neointimal
hyperplasia (Other) / restenosis (Other)},
cin = {Animal Facility (Mouse) München},
ddc = {610},
cid = {I:(DE-2719)1140012},
pnm = {352 - Disease Mechanisms (POF4-352)},
pid = {G:(DE-HGF)POF4-352},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:34869956},
pmc = {pmc:PMC8617545},
doi = {10.1016/j.jacbts.2021.06.006},
url = {https://pub.dzne.de/record/163653},
}