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Dissecting renal metabolic reprogramming heterogeneity to target kidney fibrosis

Project description

Metabolic reprogramming and chronic kidney disease

Chronic kidney disease (CKD) is associated with progressive and irreversible loss of kidney function, which ultimately leads to renal failure and end-stage kidney disease. One of the hallmarks of CKD is fibrosis, which stems from the accumulation of extracellular matrix (ECM) components upon irregular activation of myofibroblasts. Funded by the Marie Skłodowska-Curie Actions programme, the MetaboKID project focuses on the role of cellular metabolism during fibrosis. Researchers will investigate how metabolic rewiring in myofibroblasts influences fibrosis and CKD. Using advanced multi-omics, computational analyses, and innovative in vitro systems, the research seeks to develop metabolism-based therapies for CKD.

Objective

Chronic kidney disease (CKD) affects 10% of the population and fibrosis driven by excessive accumulation of extracellular matrix (ECM) is the hallmark of CKD. Myofibroblasts are the key ECM producing cells and are activated by cross-talk with injured proximal tubule anChronic kidney disease (CKD) affects 10% of the population and fibrosis driven by excessive accumulation of extracellular matrix (ECM) is the hallmark of CKD. Myofibroblasts are the key ECM producing cells and are activated by cross-talk with injured proximal tubule and immune cells. Although a derangement in fatty acid oxidation (FAO) of tubular epithelium is crucial in the pathophysiology of CKD, the metabolic rewiring of kidney myofibroblasts remains elusive. Our preliminary observations suggest that cell type-specific metabolic shifts could define new cellular subpopulations with a differential role in the fibrogenic response. To understand this, the following objectives have been defined: 1. To decipher the role of FAO in myofibroblasts during kidney fibrosis; 2.To dissect metabolic changes as important drivers of kidney fibrosis and CKD; 3. To validate key metabolic pathways in complex ex vivo models of kidney fibrosis. To address these aims, I will map the genetic and metabolic spatio-temporal features of kidney fibrosis by a combination of cutting-edge multi-omics technologies at large scale (Spatial single cell ATAC sequencing for transcriptomics and Space M for metabolomics). This will be complemented by advanced computational analyses and modeling, using CKD human biopsies and mouse renal samples from available genetic models for myofibroblast tracing and FAO enhancement. Innovative in vitro systems (cell coculture and kidney organoid systems) will be used to identify and target cell type-specific metabolic reprogramming. Strategies based on the modulation of these metabolic shifts will provide a firm basis for novel, metabolism-oriented therapeutic approaches against renal fibrosis and CKD.

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HORIZON-TMA-MSCA-PF-EF - HORIZON TMA MSCA Postdoctoral Fellowships - European Fellowships

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(opens in new window) HORIZON-MSCA-2023-PF-01

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Coordinator

UNIVERSITAETSKLINIKUM AACHEN
Net EU contribution

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€ 173 847,36
Address
Pauwelsstrasse 30
52074 Aachen
Germany

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Region
Nordrhein-Westfalen Köln Städteregion Aachen
Activity type
Higher or Secondary Education Establishments
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Total cost

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