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Regulation of the L-arginine – ADMA – Nitric Oxide (NO) Pathway in the Pulmonary Vascular Response to Hypoxia and its Role for Survival of High-Risk COPD Patients

Project description

Earlier diagnoses of high-risk COPD

Chronic obstructive pulmonary disease (COPD) is characterised by lung damage that results in airway inflammation, limiting airflow. Intermittent hypoxaemia (intermittent low oxygen levels in the blood), which often occurs with sleep apnoea, is a driver of lung function decline. The ERC-funded NO PRESSURE project will investigate whether intermittent hypoxaemia is a key driver of pulmonary pathophysiology without clinical symptoms in the early disease stages of some COPD patients at high risk of rapid pulmonary decline. With a focus on the L-arginine asymmetric dimethylarginine nitric oxide (L-arginine-ADMA-NO) pathway, the team aims to enable the use of exercise-induced intermittent hypoxaemia to identify high-risk COPD patients and pave the way to pharmacotherapeutic interventions targeting the L-arginine-ADMA-NO pathway.

Objective

NO PRESSURE will address the hypothesis that intermittent hypoxaemia is a major driver of the pulmonary pathophysiology and the systemic co-morbidity that is present at a sub-clinical level already in early disease stages of a significant sub-group of COPD patients with a high risk of rapidly declining lung function and poor prognosis.

The project has been conceptualized to achieve ground-breaking scientific insight into the role of intermittent hypoxaemia as a driver of COPD progression and outcome via dysfunction of the L-arginine-ADMA-NO pathway. Its five work packages will span from molecular regulation of the pulmonary L-arginine-ADMA-NO pathway in hypoxia to cellular oxygen sensing and signal transduction mechanisms, via translational studies in genetically modified mouse models and genotyped healthy humans, to clinical proof-of-concept studies of exercise-induced, intermittent hypoxaemia as a diagnostic indicator to identify a subgroup of high-risk COPD patients and the ability to therapeutically intervene by pharmacological modification of the L arginine-ADMA-NO pathway.

Combining state-of-the-art molecular biology techniques, specifically designed genetically engineered animal models, and translation of the obtained results into genomically characterized humans who will be exposed to hypoxia, NO PRESSURE will achieve a unique level of depth in our understanding of the molecular pathophysiology of the lung’s response to hypoxia with proven relevance to human biology. Beyond this, NO PRESSURE will take the step towards validation of pathophysiologically proven biomarkers and, thus, molecular mechanisms in the world’s unique long-term prospective cohort for lung disease. In addition, it will deliver unequivocal evidence for clinical utility in two small, but well defined COPD patient cohorts, with one having a focus on prognostic relevance and the other one opening the avenue towards future pharmacotherapeutic intervention to improve prognosis.

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Topic(s)

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HORIZON-ERC - HORIZON ERC Grants

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Call for proposal

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(opens in new window) ERC-2022-ADG

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Host institution

UNIVERSITAETSKLINIKUM HAMBURG-EPPENDORF
Net EU contribution

Net EU financial contribution. The sum of money that the participant receives, deducted by the EU contribution to its linked third party. It considers the distribution of the EU financial contribution between direct beneficiaries of the project and other types of participants, like third-party participants.

€ 2 499 927,00
Address
Martinistrasse 52
20251 Hamburg
Germany

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Region
Hamburg Hamburg Hamburg
Activity type
Higher or Secondary Education Establishments
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Total cost

The total costs incurred by this organisation to participate in the project, including direct and indirect costs. This amount is a subset of the overall project budget.

€ 2 499 927,00

Beneficiaries (1)

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