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Viviana I. Pérez

Aging biologist who studied protein homeostasis in long-lived species and how rapamycin and dietary restriction act in mice, and who now directs the National Institute on Aging's Division of Aging Biology

Director, Division of Aging Biology, National Institute on Aging · Assistant Professor, Department of Biochemistry & Biophysics, and Principal Investigator, Linus Pauling Institute, Oregon State University · postdoc, Barshop Institute for Longevity and Aging Studies, UT Health Science Center at San Antonio (2004–2011) · PhD, University of Chile (2004)

Division of Aging Biology, National Institute on Aging, NIH (Bethesda, Maryland, USA) ↗

Viviana Pérez was the senior author of the Atlas study in which her Oregon State group showed that rapamycin lowers the inflammatory secretory profile of senescent cells (SASP) without the transcription factor Nrf2, but needs Nrf2 to lower the cell-cycle brakes p16 and p21 (WAN2017). The work used mouse and human fibroblasts and a short dosing study in Nrf2-knockout mice.

Pérez trained as a pharmaceutical chemist and earned her PhD at the University of Chile, then spent seven years as a postdoctoral fellow at the Barshop Institute in San Antonio, where she worked on oxidative stress and protein stability in long-lived species such as the naked mole-rat. At the Linus Pauling Institute her lab compared protein homeostasis in long- and short-lived species and tested whether rapamycin and dietary restriction act through the same mechanism in mice. She later moved to the National Institute on Aging, where she directs the Division of Aging Biology.

Milestones in the Atlas

A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.

YearEvidenceStudy
2017 M Rapamycin inhibits the secretory phenotype of senescent cells by a Nrf2-independent mechanism WAN2017 Senior author: led the study separating rapamycin's Nrf2-independent effect on the SASP from its Nrf2-dependent effect on p16 and p21.

Co-authors in the Atlas

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