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May 24-25, 2018
London, UK
Vascular Surgery 2018
3
rd
Edition of World Congress & Exhibition on
Vascular Surgery
Journal of Vascular and Endovascular Therapy
ISSN: 2573-4482
T
he evolution of abdominal aortic aneurysm (AAA) is
unpredictable. Moreover, no specific treatment exists for AAA,
except surgery to prevent aortic rupture. Galectin-3 has been
previously associated with cardiovascular disease (CVD), but its
potential role in AAA has not been addressed. Galectin-3 levels
were increased in plasma of AAA patients (n=225) compared
to controls (n=100). Moreover, galectin-3 concentrations were
associated with need for surgical repair, independently of
potential confounding factors. Galectin-3 mRNA and protein
expression were increased in human AAA samples compared to
healthy aortas. Experimental AAA in mice was induced by aortic
elastase perfusion. Mice were treated intravenously with the
galectin-3 inhibitor modified citrus pectin (MCP, 10 mg/kg, every
other day) or saline. Similar to humans, galectin-3 serum and
aortic mRNA levels were also increased in elastase-induced AAA
mice compared to control mice. Mice treated with MCP showed
decreased aortic dilation, as well as elastin degradation, vascular
smooth muscle cell (VSMC) loss and macrophage content at
day 14 post-elastase perfusion compared with control mice. The
underlying mechanism(s) of the protective effect of MCP was
associated with a decrease in galectin-3 and cytokine (mainly
CCL5) mRNA and protein expression. Interestingly, galectin-3
induced CCL5 expression by a mechanism involving STAT3
activation in VSMC. Accordingly, MCP treatment decreased
STAT3 phosphorylation in elastase-induced AAA. In conclusion,
increased galectin-3 levels are associated with AAA progression,
while galectin-3 inhibition decreased experimental AAA
development. Our data suggest the potential role of galectin-3 as
a therapeutic target in AAA
Recent Publications
1. Dale M A, Ruhlman M K and Baxter B T (2015)
Inflammatory cell phenotypes in AAAs: their role and
potential as targets for therapy. Arterioscler Thromb
Vasc Biol 35:1746-55.
2. DanielsLB, CloptonP, LaughlinGA,Maisel ASandBarrett
Connor E (2014) Galectin-3 is independently associated
with cardiovascular mortality in community-dwelling
older adults without known cardiovascular disease: the
Rancho Bernardo study. Am Heart J 167:674-82.
3. Filipe M D, Meijers W C, Rogier van der Velde A and de
Boer R A (2015) Galectin-3 and heart failure: prognosis,
prediction & clinical utility. Clin Chim Acta 443:48-56.
4. Jagodzinski A, Havulinna AS, Appelbaum S, Zeller
T, Jousilahti P, Skytte Johanssen S, Hughes M F,
Blankenberg S and Salomaa V (2015) Predictive value of
galectin-3 for incident cardiovascular disease and heart
failure in the population-based FINRISK 1997 cohort. Int
J Cardiol 192:33-9.
5. Maiolino G, Rossitto G, Pedon L, Cesari M, Frigo A C,
Azzolini M, Plebani M, and Rossi G P (2015) Galectin-3
predicts long-term cardiovascular death in high-risk
patients with coronary artery disease. Arterioscler
Thromb Vasc Biol 35:725-3.
Biography
Mónica MTorres Fonseca is a Vascular Surgeon who, along with her clinical
work, devotes a large part of her time to the field of research, which she is
passionate about. She and her group’s work are mainly directed to the study
of AAA for years. This is the object of study in her doctoral thesis, based on
the diagnosis, prognosis and treatment of AAA through clinical and exper-
imental studies. She is concerned about the situation of patients with AAA
without surgical indication, who cannot be offered effective medical treat-
ment at this time. Therefore, part of their study aims to determine possible
particles that can reduce or delay the progression of the aneurysm, which
would mean a substantial change in the prognosis of these patients.
monitorfon@gmail.comIncreased galectin-3 levels are associated with abdominal
aortic aneurysm progression and inhibition of galectin-3
decrease elastase-induced AAA development
Mónica M Torres Fonseca
Autonomous University of Madrid, Spain
Mónica M Torres Fonseca, J Vasc Endovasc Therapy 2018, Volume 3
DOI: 10.21767/2573-4482-C1-002