Mikhail V. Blagosklonny
Proposes the hyperfunction theory: TOR signaling that builds a young body never fully switches off, and drives its aging instead
MD & PhD, Pavlov First State Medical University, St. Petersburg · Fogarty Fellowship, NIH · NCI, Univ. of Pennsylvania, New York Medical College, Ordway Research Institute · Professor of Oncology, Roswell Park Comprehensive Cancer Center, Buffalo (2009–2024) · founding Editor-in-Chief, Cell Cycle, Aging, Oncotarget, Oncoscience · died October 2024
In memoriam / Aging (Aging-US) editor profile ↗
In 2009 (DEM2009), showed that blocking a cell's division while mTOR keeps driving growth tips it into permanent senescence — rapamycin uncouples growth from division, keeping arrest reversible. This anchored his 2006 theoretical paper (BLA2006) proposing the 'hyperfunction theory' of aging: growth-driving TOR signaling stays 'quasi-programmed' on past development and drives age-related disease.
Trained as a physician-scientist in Russia, moved through NIH, NCI, Penn, NYMC, Ordway before Roswell Park (2009). Founded and edited Cell Cycle, Aging, Oncotarget, Oncoscience — shaping how much of the geroscience field published for over a decade.
A polarizing, outspoken figure who publicly took rapamycin himself and advocated it for healthy people, well ahead of completed human trials — a position most of the field still treats as premature. Died October 2024 of metastatic lung cancer; over 290 peer-reviewed papers.
Milestones in the Atlas
| Year | Evidence | Study |
|---|---|---|
| 2006 | R | Aging and immortality: quasi-programmed senescence and its pharmacologic inhibition BLA2006 Proposes the hyperfunction theory of aging. |
| 2009 | M | Rapamycin decelerates cellular senescence DEM2009 Shows the key experiment: blocking division while mTOR keeps driving growth tips cells into permanent senescence; rapamycin keeps arrest reversible. |