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Deciphering the role of adipose tissue in cardiac health and disease: ADIPOhealth

Project description

Adipose-heart communication in obesity

Obesity is a major risk of heart diseases, but how fat accumulation affects cardiovascular function remains poorly understood. The ERC-funded ADIPOhealth project will study the underlying molecular and physiological mechanisms through which dysfunctional adipose tissue, commonly known as body fat, leads to cardiometabolic impairment. It focuses on metabokines released by fat tissue, such as proteins, metabolites, microRNAs and extracellular vesicles that may alter heart metabolism and function. By combining multi-omics data, cellular models and mouse studies, the project aims to identify key molecules involved in this cross-talk, understand their role in heart disease. The goal is to explore new strategies to prevent or treat cardiometabolic disorders.

Objective

Obesity is a major risk factor for cardiovascular diseases (CVD), primarily due to its disruption of heart metabolism and the alteration of crucial signaling pathways involved in maintaining cardiac function, including those regulating energy homeostasis, myocardial contractility, and stress response. Nevertheless, the underlying mechanisms for these effects remain poorly understood. Obesity leads to changes in the secretion, by adipose tissue (AT), of metabokines—proteins, peptides, metabolites, and extracellular vesicles (EVs)—that are critical for inter-organ communication and significantly affect heart function.
AT is a key endocrine organ involved in whole-body homeostasis, yet its impact on cardiac health is still not fully understood. We hypothesize that AT dysfunction is a key driver of heart disease through disrupted metabokine secretion. Our preliminary findings suggest that specific AT alterations profoundly affect heart metabolism and function. ADIPOhealth aims to advance our understanding of how AT controls cardiac function through the following objectives:
1. Identify novel metabokines (adipokines, metabolites, microproteins, microRNAs, and EVs) secreted by AT that contribute to the development of heart disease.
2. Discover novel metabokines that regulate cardiomyocyte metabolism using cellular models.
3. Investigate, in mouse models of AT-specific dysfunction, how cardiac function may be influenced by changes in metabokines.
4. Functionally characterize these metabokines in cell culture, mouse models, and human samples.
5. Develop therapeutic strategies targeting AT dysfunction and metabokine-induced cardiac damage.
By integrating multi-omics data from human and mouse studies, we aim to elucidate the molecular mechanisms by which AT influences heart health. Our results not only will deepen our understanding of metabolic crosstalk between organs but will also identify new therapeutic targets to combat cardiometabolic diseases (CMDs).

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Programme(s)

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Topic(s)

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Funding Scheme

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HORIZON-ERC-SYG - HORIZON ERC Synergy Grants

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Call for proposal

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(opens in new window) ERC-2025-SyG

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Host institution

FUNDACION SECTOR PUBLICO ESTATAL CENTRO NACIONAL INVESTIGACIONES ONCOLOGICAS CARLOS III
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.

€ 3 300 500,00
Address
C MELCHOR FERNANDEZ ALMAGRO 3
28029 Madrid
Spain

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Region
Comunidad de Madrid Comunidad de Madrid Madrid
Activity type
Research Organisations
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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.

€ 3 300 500,00

Beneficiaries (5)