George Kelly
Cell biologist from Viktor Korolchuk's group at Newcastle University who showed that the routine clearing of damaged mitochondria fails as human cells become senescent
Biosciences Institute, Newcastle University (PubMed affiliation 2020–2024, Korolchuk lab, at the time of the study)
Mitochondria are the power stations of the cell, and damaged ones are removed by a process called mitophagy. George Kelly is first author of the 2024 Developmental Cell study in this Atlas (KEL2024). In healthy primary human cells, mitophagy ran at a steady high level, started by superoxide made in the mitochondria and carried out through the PINK1/Parkin pathway with p62 as the receptor that tags mitochondria for removal. This housekeeping shut down when cells became senescent, the non-dividing state that builds up with age, and in cells from older donors. Blocking mitophagy in young cells was enough to push them into senescence.
The study also matters for rapamycin. Turning mitophagy back on was needed for rapamycin and NAD precursors to hold back senescence, which suggests that part of rapamycin's effect on cell aging works through mitochondrial quality control. A small molecule that targets p62 could restore mitophagy and reverse aging features in the cells. All of this was shown in cultured human cells.
PubMed links Kelly to Viktor Korolchuk's group at Newcastle University from 2020, starting with a review on reactive oxygen species and autophagy in neurons. Kelly is also a co-author of a 2022 Developmental Cell paper from the same lab showing that autophagy keeps cells alive by maintaining NAD levels, of a 2022 eLife study on short senolytic treatments in irradiated mice, and of a 2023 Nature paper with Joao Passos on how stressed senescent cells release mitochondrial DNA. A current position could not be confirmed.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2024 | M | Suppressed basal mitophagy drives cellular aging phenotypes that can be reversed by a p62-targeting small molecule KEL2024 First author: showed that basal mitophagy shuts down in senescent and aged human cells and that its return is needed for rapamycin's anti-senescence effect. |
Co-authors in the Atlas 6
People with a profile here who share at least one study with George Kelly.
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- Bernadette Carroll First author of the study showing why mTORC1 stays switched on in senescent cells, and co-author on G3BP–TSC and senescence-mitophagy work; her own lab studies how nutrient sensing breaks down in ageing cells.
- Glyn Nelson Microscopy specialist who manages Newcastle University's Bioimaging Unit and has worked for many years on the signalling networks that keep senescent cells in their arrested state
- Penny Lovat Professor of Cellular Dermatology and Oncology at Newcastle University who studies autophagy in melanoma, and whose work on the autophagy protein AMBRA1 and the skin protein loricrin underlies a test, developed with AMLo Biosciences, to identify early melanomas at low risk of spreading
- Satomi Miwa Mitochondrial biologist who contributed to Newcastle studies on rapamycin in NF-κB-driven ageing mice and on basal mitophagy as a brake on cellular senescence.
- Thomas von Zglinicki Cell-senescence researcher who co-authored the Newcastle studies on stuck-on mTORC1 in senescent cells and on loss of basal mitophagy as a driver of cellular ageing.
- Viktor I. Korolchuk Showed that where lysosomes sit inside the cell tunes mTORC1 activity to nutrient supply. His Newcastle lab found that senescent cells can no longer switch mTORC1 off when nutrients or growth factors are withdrawn, and studies how autophagy and mitophagy decline with age
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