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Manuel prota
Manuel prota










manuel prota

The cookie is used to store the user consent for the cookies in the category "Performance". This cookie is set by GDPR Cookie Consent plugin. The cookies is used to store the user consent for the cookies in the category "Necessary". The cookie is used to store the user consent for the cookies in the category "Other. The cookie is set by GDPR cookie consent to record the user consent for the cookies in the category "Functional". The cookie is used to store the user consent for the cookies in the category "Analytics". These cookies ensure basic functionalities and security features of the website, anonymously. Necessary cookies are absolutely essential for the website to function properly. The ultimate goal is to improve the therapeutic outcome of senescence-associated diseases by developing new strategies for the detection and elimination of senescent cells in patients. This project will study CypD as a novel, non-invasive senolytic target and provide a molecular understanding of its modulation in senescence biology, taking advantage of the various well-established senescence models developed in Serrano’s laboratory, including human and mouse cells and in vivo models. Interestingly, additional functions have been described for CypD, including proteins scaffolding, as it binds to several mitochondrial proteins, apoptosis and mitophagy control, and regulation of the electron transport chain activity. CypD is a matrix isomerase involved in various mitochondrial functions, including the regulation of cell death and the opening of the mitochondrial permeability transition pore, a non-specific pore in the inner mitochondrial membrane, by sensitising it to calcium and reactive oxygen species. Through a CRISPR/Cas9-based screening, Serrano’s laboratory identified Cyclophilin D (CypD) as a promising candidate target, since its inactivation leads to the selective elimination of senescent cells while being non-toxic for control proliferating cells. Abundant evidence highlights how changes in mitochondria and cellular metabolism can be both cause and consequence of the senescent phenotype and suggests a possible role of this organelle in the specific targeting of these cells.

manuel prota

While the selective elimination of senescent cells is a primary therapeutical goal in the field, no clinically approved treatment currently exists, which constitutes an important research gap. Ageing-related diseases are tightly correlated with the accumulation of senescent cells.












Manuel prota