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Investigating the regulation of the senescence-associated secretory phenotype (SASP) by mitochondrial DNA (mtDNA) metabolism for the development of novel senotherapies.

Project description

Mitochondrial DNA and cell senescence

Cellular senescence is a stress response that involves irreversible proliferative arrest and the expression of inflammatory factors known as the senescence-associated secretory phenotype (SASP). While senescence acts as a tumour-suppressing mechanism by limiting the proliferation of potentially cancerous cells, the accumulation of senescent cells in ageing and disease can lead to harmful effects, particularly due to the SASP. With the support of the Marie Skłodowska-Curie Actions programme, the MitoDNASen project aims to explore the role of mitochondrial DNA (mtDNA) maintenance in SASP expression, as alterations in mtDNA and its replication have been linked to senescence. Preliminary results suggest that increased mtDNA copy number promotes SASP expression. The goal is to identify potential targets to modulate SASP and mitigate the negative impact of senescent cells.

Objective

In response to various stresses such as DNA damage, telomere erosion, or oncogene activation, human cells can enter senescence. This process is characterized by irreversible proliferative arrest, deep transcriptional reprogramming, and expression of a collection of inflammatory factors termed the SASP (senescence-associated secretory phenotype). As it limits the proliferation of cells potentially bearing neoplastic potential, the triggering of cellular senescence is an essential tumor suppressing mechanism. However, the persistence and accumulation of senescent cells in aging and pathological contexts can have deleterious effects, particularly due to the SASP. It is thus fundamental to understand the basic physiology of senescent cells to develop so-called senomorphic drugs that modulate SASP expression. Changes in mitochondrial physiology elicited during cellular senescence onset strongly suggest that the maintenance and integrity of their mitochondrial DNA (mtDNA) may be altered. For instance, cytosolic leakage of mtDNA has been shown to take place in senescent cells and participate in SASP expression via immune pathways activation, but the contribution of mtDNA metabolism and replication in SASP expression has not yet been explored. My preliminary results show that mtDNA copy number increases continuously during senescence progression, accompanied by recomposing of the mitochondrial replisome. I also showed that this increase in mtDNA copy number promotes SASP expression. In the present project, I will characterize in details the alterations in mtDNA maintenance and integrity during senescence; profile the evolution of mitochondrial replisome composition; and characterize how the previous regulate SASP expression. The perspective of this project is to identify new senomorphic targets for controlling SASP expression and hereby alleviate the adverse effects of senescent cells in pathological contexts.

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

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Call for proposal

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

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Coordinator

UMEA UNIVERSITET
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.

€ 206 887,68
Address
UNIVERSITETOMRADET
901 87 UMEA
Sweden

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Region
Norra Sverige Övre Norrland Västerbottens län
Activity type
Higher or Secondary Education Establishments
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Total cost

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