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Mechano-Ageing

Financiado

Role of extracellular matrix as regulator of ageing through mechanosignaling

"A recent work published by the host laboratory had redefined aging as a mechano-disease. Transcriptional co-factors YAP/TAZ, masters of mechanotransduction, were critical in stromal cells to prevent aging. Importantly, restoring... ver más

31/08/2026

UNIPD

189K€

Presupuesto del proyecto: 189K€

Líder del proyecto

UNIVERSITA DEGLI STUDI DI PADOVA No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Financiación concedida El organismo HORIZON EUROPE notifico la concesión del proyecto el día 2023-05-11

HORIZON-MSCA-2022-PF-01-01: MSCA Postdoctoral Fellowships 2022 ExpectedOutcome:

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Cerrada hace 2 años

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Información adicional privada

No hay información privada compartida para este proyecto. Habla con el coordinador.

1 Participantes

UNIPD

188.59K€ | Lider

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Duración del proyecto: 39 meses Fecha Inicio: 2023-05-11
Fecha Fin: 2026-08-31

Líder del proyecto

UNIVERSITA DEGLI STUDI DI PADOVA No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 189K€

Descripción del proyecto "A recent work published by the host laboratory had redefined aging as a mechano-disease. Transcriptional co-factors YAP/TAZ, masters of mechanotransduction, were critical in stromal cells to prevent aging. Importantly, restoring cell-ECM communication and YAP/TAZ level was sufficient to ""rejuvenate"" old cells. Consequently, we hypothesize that the culprit of aging should be searched in ECM changes that drive the loss of mechanotransduction in stromal cells. Using single cell RNA-sequencing data of mouse dermal fibroblasts and mass-spec analyses of the dermis ECM during aging, we will seek for ECM candidates that may be at the root of this process. Then, we will build an Atlas of the mouse skin during aging using spatial transcriptomic and immunolabeling of mechanoresponsive proteins to unveiled new interconnections between the ECM and altered mechanotransduction during aging. As validation, we will use two complementary in vitro approaches. First, old mice fibroblasts will be culture on a young ECM synthetized by engineered young mice fibroblast lacking specific ECM genes, pinpointing to ECM proteins able to rejuvenate old cells. Second, we will generate 3D organotypic skin culture with keratinocytes and engineered dermal fibroblast lacking specific ECM candidate. We will ask whether it affects mechanosignaling and acquisition of aging traits in both dermis and epidermal compartments. Digging into the mechanics of aging is crucial because it would add a new paradigm on the causes of cell senescence and aging, define new markers for healthy aging and inform on new therapeutic perspectives to combat aging or some of its associated pathologies."

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