"The role of the GPR55/LPI system in cardiovascular physiology and pathology"

Rejestracja

strona www: www.jcet.eu

Termin i miejsce

01.04.2016 − Sala Ateńska, budynek A, Park Life Science, Bobrzyńskiego 14, Kraków, woj. małopolskie

Komitety

Przewodniczący komitetu naukowego:
Prof. Cherry Wainwright (Robert Gordon University, Aberdeen, UK)

Organizatorzy

Jagiellońskie Centrum Rozwoju Leków(JCET) Uniwersytet Jagielloński

Tematyka

GPR55 is a recently de-orphanised receptor, whose endogenous ligand is the
lysophospholipid, lysophosphatidyl inositol (LPI). GPR55 has been implicated to play a
role in numerous physiological and pathophysiological processes such as cancer and
diabetes, but to date relatively little is known about its involvement in the
cardiovascular system. My group has been studying the GPR55/LPI system in
cardiovascular physiology and our recently published data has shown that a
dysfunctional GPR55/LPI system results in reduced cardiac systolic function and
contractile reserve, an effect that may be related to impaired sympathetic nervous
activity. More recently we have shown that LPI exacerbates the extent of injury
following acute myocardial ischaemia and reperfusion, signalling via the RhoA/ROCK
pathway. We have also explored the role of GPR55 in the development of obesity and
metabolic syndrome, and the impact of this on cardiovascular function and injury
sustained following myocardial ischaemia/reperfusion. In terms of the vasculature, we
have also investigated the importance of GPR55 in the setting of atherogenesis, in terms
of vascular endothelial function, atheroma development and dyslipidaemia-induced
cardiac impairment. In my lecture I will summarise this data and provide evidence for an
essential role of the GPR55/LPI system in cardiovascular and metabolic physiology.
The role of the GPR55/LPI system in
cardiovascular physiology and pathology

Dodatkowe informacje

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