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Cellular senescence is a highly stable cell cycle arrest that limits the replication of aged or damaged cells. Senescence can be triggered by replicative exhaustion, oncogene activation or chemotherapeutic drugs. As a consequence, senescence influences the outcome of physiological processes such as aging, development, wound healing, fibrosis and cancer. Recently, strategies aimed to selectively eliminate senescent cells (senolytic therapies) have been shown great promise for the treatment of a wide-range of diseases. Senescent cells not only exit cell cycle but also undergo profound changes in their transcriptional program, chromatin organization, metabolism and secretome. In particular, the senescence-associated secretory phenotype (SASP) mediates many of the patho-physiological effects exerted by senescent cells.
The goal of our research program is to understand the molecular mechanisms behind the implementation and regulation of senescence. To this end, we use different human primary cell systems, including IMR90 ER:RAS cells as an inducible system of oncogene-induced senescence. Our experimental approaches integrate information from shRNA functional screenings, cellular and molecular biology, high-throughput microscopy, genomics and proteomics that we aim to translate to disease-relevant mouse models.
There are three general questions questions that we are aiming to address:
What are the epigenetic mechanisms controlling senescence?
What are the regulation, composition and functions of the senescence secretome?
How can we target senescent cells for therapeutic benefit in cancer and aging?
Overall, we expect that our research would result in a better knowledge of how senescence impacts aging, cancer and other diseases, opening possibilities to manipulate it for therapeutic advantage.
The goal of our research program is to understand the molecular mechanisms behind the implementation and regulation of senescence. To this end, we use different human primary cell systems, including IMR90 ER:RAS cells as an inducible system of oncogene-induced senescence. Our experimental approaches integrate information from shRNA functional screenings, cellular and molecular biology, high-throughput microscopy, genomics and proteomics that we aim to translate to disease-relevant mouse models.
There are three general questions questions that we are aiming to address:
What are the epigenetic mechanisms controlling senescence?
What are the regulation, composition and functions of the senescence secretome?
How can we target senescent cells for therapeutic benefit in cancer and aging?
Overall, we expect that our research would result in a better knowledge of how senescence impacts aging, cancer and other diseases, opening possibilities to manipulate it for therapeutic advantage.
研究兴趣
论文共 178 篇作者统计合作学者相似作者
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Imanol Duran, Joaquim Pombo, Bin Sun,Suchira Gallage,Hiromi Kudo,Domhnall McHugh, Laura Bousset, Jose Efren Barragan Avila,Roberta Forlano,Pinelopi Manousou, Mathias Heikenwalder,Dominic J. Withers,
Nature Communicationsno. 1 (2024): 1-20
Jesús Gil, Preeti Kerai,Matilde Lleonart,David Bernard,Juan Cruz Cigudosa,Gordon Peters, Amancio Carnero,David Beach
crossref(2023)
Agingno. 7 (2023): 2369-2370
Christina Guo,Adam Sharp,Bora Gurel,Mateus Crespo,Ines Figueiredo,Suneil Jain, Ursula Vogl,Jan Rekowski, Mahtab Rouhifard,Lewis Gallagher,Wei Yuan,Suzanne Carreira,
Natureno. 7989 (2023): 1-3
Hiroshi Kondoh,Matilde E. Lleonart,Jesus Gil, Jing Wang,Paolo Degan,Gordon Peters,Dolores Martinez, Amancio Carnero, David Beach
crossref(2023)
Hiroshi Kondoh,Matilde E. Lleonart,Jesus Gil, Jing Wang,Paolo Degan,Gordon Peters,Dolores Martinez, Amancio Carnero, David Beach
crossref(2023)
Nicolas Humbert, Sébastien Martien,Arnaud Augert,Marco Da Costa, Sébastien Mauen,Corinne Abbadie,Yvan de Launoit,Jesús Gil,David Bernard
crossref(2023)
Anissa A. Widjaja,Wei‐Wen Lim, V. Sivakumar,Sonia Chothani,Ben Corden,Joyce Wei Ting Goh,Jessie Tan,Chee Jian Pua,Radiance Lim,Brijesh Kumar Singh,Dasan Mary Cibi, Susanne Weber,
bioRxiv (Cold Spring Harbor Laboratory) (2023)
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Nature cell biologyno. 11 (2023): 1554-1556
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