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Cardiac Uptake REstoration of Glucose in diabetic Heart Failure

Project description

Glucose uptake restoration in diabetic and heart failure patients

Heart failure (HF) affects over 64 million people, with 40 % also having type 2 diabetes. Current HF treatments often ignore metabolic issues. A newly identified gene, more active in those with both conditions, HF and diabetes, influences glucose uptake. Reducing this gene’s expression improves glucose control and cardiac function in mice with heart failure on a high-fat diet. The ERC-funded CURE-HF project will develop safe, selective small molecules to inhibit this gene. It will validate promising compounds in both human iPSC-derived cardiomyocytes and diabetic HF mouse models. Targeting the energy deficit in diabetic HF could lead to therapies that reduce hospitalisations and enhance patient outcomes.

Objective

Heart failure (HF) affects over 64 million people worldwide and is a leading cause of hospitalization and premature death. About 40% of HF patients also have type 2 diabetes, doubling mortality risk. In HF, the stressed myocardium shifts toward glucose metabolism, but in diabetes cardiomyocytes fail to take up glucose and remain reliant on fatty acids, leaving the heart energy-starved. Current HF therapies target neurohormonal pathways to reduce workload and slow progression but do not address this root metabolic defect. Insulin and GLP-1 receptor agonists can influence glucose metabolism, but their use in HF is limited by side effects, lack of direct cardiac efficacy, or even potential harm.

CURE-HF proposes a novel approach by developing small-molecule inhibitors of a newly identified gene. Patient data revealed that this gene was the most differentially expressed in patients with heart failure and diabetes compared to heart failure patients without diabetes. Knockdown of this gene in hiPSC-derived cardiomyocytes increased glucose uptake, while mice lacking this gene on a high-fat diet with induced HF had better glucose control and 20% higher myocardial glucose uptake by FDG-PET and a better cardiac function. These findings demonstrate that inhibition of this gene restores energy balance and protects against diabetic HF.

Building on these insights, CURE-HF will design and optimise selective, safe, and synthetically accessible small molecules to inhibit the newly identified gene. Lead compounds will be validated in human iPSC-cardiomyocytes and in diabetic HF mouse models, with functional readouts including glucose uptake, echocardiography, and FDG-PET. In parallel, the project will secure IP, engage stakeholders, and assess market potential.

By addressing the root energetic deficit of diabetic HF, CURE-HF has the potential to deliver a disease-modifying small-molecule therapy, reduce hospitalization and improve prognosis.

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HORIZON-ERC-POC - HORIZON ERC Proof of Concept Grants

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Call for proposal

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(opens in new window) ERC-2025-POC

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Host institution

ACADEMISCH ZIEKENHUIS GRONINGEN
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.

€ 150 000,00
Address
HANZEPLEIN 1
9713 GZ Groningen
Netherlands

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Activity type
Higher or Secondary Education Establishments
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Total cost

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Beneficiaries (1)

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