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MOLEC ANTI-ARRHYT SIGNED

Resilience and Trigger Factors in Cardiac Arrhythmia: Risk Stratification and Drug Design

Total Cost €

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EC-Contrib. €

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Partnership

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 MOLEC ANTI-ARRHYT project word cloud

Explore the words cloud of the MOLEC ANTI-ARRHYT project. It provides you a very rough idea of what is the project "MOLEC ANTI-ARRHYT" about.

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Project "MOLEC ANTI-ARRHYT" data sheet

The following table provides information about the project.

Coordinator
LINKOPINGS UNIVERSITET 

Organization address
address: CAMPUS VALLA
city: LINKOPING
postcode: 581 83
website: n.a.

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country Sweden [SE]
 Total cost 1˙499˙998 €
 EC max contribution 1˙499˙998 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2019-STG
 Funding Scheme ERC-STG
 Starting year 2020
 Duration (year-month-day) from 2020-03-01   to  2025-02-28

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    LINKOPINGS UNIVERSITET SE (LINKOPING) coordinator 1˙499˙998.00

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 Project objective

Up to 30% of individuals with inherited cardiac arrhythmias such as Long QT syndrome are not protected from sudden cardiac death despite state-of-the-art treatment. A major hurdle for effective risk stratification and treatment of inherited cardiac arrhythmias is the poor correlation between genetic variant and clinical manifestations. Affected individuals, who harbour the same arrhythmia-causative mutation, paradoxically display a spectrum of clinical phenotypes ranging from a lifelong asymptomatic state to sudden death in infancy. Up to 40% of genotype-positive individuals, depending on type of arrhythmia, do not display clinical manifestation. Based on our unpublished observations, I propose that an important, yet unexplored, underlying cause of the diverse clinical manifestations are endogenous resilience and trigger factors, which interact with mutated cardiac ion channels to alter arrhythmia severity. MOLEC ANTI-ARRHYT utilizes front-line experimental and computational approaches and the cardiac IKs potassium channel, which is strongly linked to lethal arrhythmias and sudden cardiac death, as a prototype. We aim to: (i) identify major classes of endogenous ligands with therapeutic (resilience factors) or pathological (trigger factors) effects on the IKs channel, (ii) provide proof of mechanism for how the effect of resilience and trigger factors is determined by arrhythmia-causative mutations in the IKs channel, (iii) utilize resilience mechanisms to develop a fundamentally novel concept of anti-arrhythmic drug development: Resilience-Mimetic Drug Development. The successful completion of this project will open up new avenues for personalized risk stratification and clinical management, which ultimately will improve the clinical outcome for individuals with inherited arrhythmias.

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