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A New Mouse Model to Study Acquired Lymphedema 英文参考文献
Perspectives
A New Mouse Model to Study
Acquired Lymphedema
Martin Schneider, Annelii Ny, Carmen Ruiz de Almodovar, Peter Carmeliet
*
M
ore than 1 million women
worldwide develop breast
cancer every year [1]. For
medical practice still relies on
ancient procedures, such as manual
lymph drainage via massage. A
hydrodynamic and cellular mechanisms
and the rate of lymph drainage in a
horizontally positioned mouse tail also
differ from those in a supine human
limb, in which positional changes and
muscle contractions determine lymph
drainage [7]. It is unclear to what
extent these differences in?uence the
disease course and severity. Moreover,
it will be interesting to characterize the
long-term chronic structural changes in
the lymphedemic mouse tail.
Interestingly, not only were lymph
vessels dilated in the mouse tail model,
but there were also 10-fold more
lymphatic vessels in the lymphedemic
tail than in control tails. It remains
to be determined whether this
increase in the number of lymphatic
vessels in the lymphedemic tissue is a
peculiarity of the mouse tail model,
as very little information about
lymphatic hyperplasia in humans
with lymphedema is available. While
the precise reason for this increased
lymphatic vessel density remains
many of them, surgical removal of
the breast remains the ?rst line of
treatment for this potentially deadly
disease. Because breast cancer cells
spread via lymph vessels, at the time
that the breast is resected, locally
involved lymph nodes in the armpit
and part of the axillary lymphatic
network are usually also removed.
Consequently, normal drainage of
lymph is often interrupted, causing
swelling of the affected arm due to
lymph accumulation—a condition
termed lymphedema. Acquired
lymphedema in humans may also result
from irradiation, trauma, or (parasitic)
infection.
better knowledge of the molecular
cues underlying the abnormalities
that characterize the in?ammatory
tissue response to lymph stagnation
is thus urgently needed to
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