Roman V. Kondratov
Showed the circadian clock protein BMAL1 gates TOR/mTOR signaling to control aging, and that calorie restriction's lifespan benefits require a working circadian clock
Professor & Associate VP for Research, Cleveland State University · Center for Gene Regulation in Health and Disease
Kondratov Lab, Center for Gene Regulation in Health and Disease, Cleveland State University (Cleveland, Ohio, USA) ↗ ORCID0000-0003-3449-745X ↗
Portrait: Cleveland State University
Roman Kondratov leads a laboratory at Cleveland State University studying how the circadian clock — the internal 24-hour timekeeping system — shapes metabolism, cardiovascular physiology, and aging. His lab reported that mice lacking BMAL1, the core circadian clock protein, develop an early-aging syndrome: a lifespan of about 9 months versus 28 months in normal mice, along with sarcopenia, osteoporosis, cataracts, and other age-related pathologies.
Because BMAL1 is a transcription factor that can influence many pathways, the lab has worked out which downstream systems carry the aging signal, including TOR signaling, the Sirtuin pathway, and IGF/IGFR signaling — pathways that govern cell growth and the organism's response to nutrients and stress. A parallel line of work in the lab established that calorie restriction, one of the most robust lifespan-extending interventions known, works partly by resetting circadian rhythms in gene expression, and that an intact circadian clock is necessary for calorie restriction to extend lifespan.
That combination of circadian timing and mTOR signaling is the throughline of the lab's more recent work, including showing that calorie restriction's effect on liver mTOR signaling is time-of-day dependent — the same theme carried into VEL2026, comparing calorie restriction to fasting-refeeding cycles.
Milestones in the Atlas
| Year | Evidence | Study |
|---|---|---|
| 2014 | A | BMAL1-dependent regulation of the mTOR signaling pathway delays aging KHA2014 Loss of the clock protein BMAL1 raised mTORC1 activity in mice and in cultured cells, and rapamycin extended the lifespan of Bmal1-/- mice by 50%. Places the circadian clock upstream of mTORC1 as a brake, and links that brake to ageing. |
| 2026 | A | Anticipatory metabolic regulation drives the distinct and improved metabolic state of caloric restriction compared to Fasting-Refeeding cycles. VEL2026 Senior/corresponding author; showed caloric restriction engages anticipatory, circadian-clock-aligned control of hepatic mTOR signaling, distinct from the reactive, cue-driven signaling seen under fasting-refeeding cycles. |
Co-authors in the Atlas
People with a profile here who share at least one study with Roman V. Kondratov.
- Nikkhil Velingkaar Postdoctoral fellow studying how the circadian clock times caloric restriction's effects on liver mTOR signaling and metabolism