Jorge I. Castillo-Quan

Castillo-Quan trained initially as a physician at the Universidad Autónoma de Yucatán in México, where his interest in the biological mechanisms underlying metabolic and age-related diseases led him toward experimental research. He subsequently completed an M.Sc. in Clinical Neuroscience at the Queen Square Institute of Neurology, University College London (UCL), followed by a Ph.D. in Genetics, Neuroscience and Biogerontology at the UCL Institute of Healthy Ageing under the mentorship of Professor Dame Linda Partridge and Professor Sir John Hardy.

During his doctoral research, Castillo-Quan investigated genetic and pharmacological mechanisms that regulate aging and longevity using Drosophila melanogaster. His work helped establish links between nutrient-sensing pathways, cellular stress responses, and longevity. Among these studies, he demonstrated that lithium promotes longevity through a GSK3/Nrf2-dependent stress response and subsequently helped show that simultaneously targeting multiple components of the nutrient-sensing network can produce additive effects on lifespan.

In 2016, Castillo-Quan joined the Joslin Diabetes Center and Harvard Medical School for postdoctoral training with the late Prof. T. Keith Blackwell and subsequently with Prof. Jean Schaffer. There, he expanded his research toward understanding how lipid metabolism, redox biology, and protein homeostasis interact to regulate cellular resilience and organismal aging, with a particular focus on the nematode Caenorhabditis elegans. His postdoctoral research was supported in part by a Glenn Foundation for Medical Research Postdoctoral Fellowship in Aging Research, and the Reboot Fund from the American Federation for Aging Research.
Castillo-Quan joined the Department of Biological Sciences at Ohio University in August 2026, where he established the CORA Laboratory to investigate the cellular and molecular mechanisms that allow organisms to maintain homeostasis during metabolic and environmental stress and how these mechanisms change during aging.

Research Interests

Cellular & Organismal Resilience and Aging Laboratory

Aging is accompanied by a progressive decline in the ability of cells and organisms to maintain homeostasis in the face of metabolic, environmental, and proteotoxic challenges. The CORA Laboratory investigates the molecular mechanisms that create cellular and organismal resilience and asks how these protective systems influence health and longevity.

Our research focuses particularly on the intersection of metabolism, redox biology, and proteostasis. Rather than studying these processes independently, we investigate how cells coordinate metabolic state with stress-responsive transcription, protein quality control, organelle function, and lipid homeostasis.

A major focus of the laboratory is understanding how lipids function as signals, rather than simply as energy stores or structural components. We investigate how changes in lipid metabolism and lipid composition influence stress-response pathways, protein homeostasis, and longevity. Particular attention is given to the functional relationship between the endoplasmic reticulum and lipid droplets, and how lipid-driven remodeling of these organelles influences cellular stress resilience.

The laboratory also investigates the SKN-1/Nrf family of transcription factors, evolutionarily conserved regulators of oxidative stress responses, detoxification, metabolism, and proteostasis. Our work seeks to understand how distinct SKN-1 isoforms sense metabolic and proteostatic perturbations and coordinate adaptive transcriptional programs. This includes investigating mechanisms controlling SKN-1A/Nrf1 through the endoplasmic reticulum and ER-associated degradation, as well as pathways regulating SKN-1C/Nrf2-like oxidative stress responses.

Additional areas of interest include nutrient-sensing pathways, autophagy and lipophagy, mitochondrial and peroxisomal metabolism, protein folding and chaperone systems, the integrated stress response, ER stress and ER-associated degradation, phospholipid metabolism, and mechanisms of metabolic ROS production.

Selected Publications

• Castillo-Quan, J.I., McCarty, A., Kurdeikaite, U., Gilmore, K., Cabral, A., Mejia, J., Barrett, J., La Terza, M., Johnson, E., Carroll, A., Blackwell, T.K., Schaffer, J.E., and Moroz, N. Krüppel-like factors regulate lipid homeostasis to modulate SKN-1/Nrf activity, oxidative stress resistance and longevity. Genetics, In press. [bioRxiv preprint, 2025; doi: 10.1101/2025.11.22.689963].
• Zhu, F., Castillo-Quan, J.I., Ogawa, T., Wu, Z., Ding, L., Sura, M., Watanabe, Y., Lentschat, H., Fernández-Cárdenas, L.P., Dag, U., Beck-Sickinger, A., Wang, M.C., Kahn, C.R., and Blackwell, T.K. (2026). Fatty acid regulation of feeding in Caenorhabditis elegans reveals the potential ancestral origin of a GLP-1-like multiagonist signaling system. Proceedings of the National Academy of Sciences USA, 123, e2530979123.
• Short, E., ICCARP, Calimport, S., and Bentley, B. (2025). Defining an ageing-related pathology, disease or syndrome: International Consensus Statement. GeroScience, 47, 1713–1720.
• Castillo-Quan, J.I., Steinbaugh, M.J., Fernandez-Cardenas, L.P., Pohl, N.K., Wu, Z., Zhu, F., et al. (2023). An antisteatosis response regulated by oleic acid through lipid droplet-mediated ERAD enhancement. Science Advances, 9, eadc8917.
• Castillo-Quan, J.I., Tain, L.S., Kinghorn, K.J., Li, L., Grönke, S., Hinze, Y., Blackwell, T.K., Bjedov, I., and Partridge, L. (2019). A triple drug combination targeting components of the nutrient-sensing network maximizes longevity. Proceedings of the National Academy of Sciences USA, 116, 20817-20819.
• Stead, E.R., Castillo-Quan, J.I., Martinez Miguel, V.E., Lujan, C., Ketteler, R., Kinghorn, K.J., and Bjedov, I. (2019). Agephagy – Adapting autophagy for health during aging. Frontiers in Cell and Developmental Biology, 7, 308. Joint first authors.
• Ewald, C.Y., Castillo-Quan, J.I., and Blackwell, T.K. (2018). Untangling longevity, dauer, and healthspan in Caenorhabditis elegans insulin/IGF-1-signalling. Gerontology, 64, 96–104.
• Castillo-Quan, J.I. and Blackwell, T.K. (2016). Metformin: Restraining nucleocytoplasmic shuttling to fight cancer and aging. Cell, 167, 1670–1671.
• Castillo-Quan, J.I., Li, L., Kinghorn, K.J., Ivanov, D.K., Tain, L.S., Slack, C., Kerr, F., Nespital, T., Thornton, J., Hardy, J., Bjedov, I., and Partridge, L. (2016). Lithium promotes longevity through GSK3/NRF2-dependent hormesis. Cell Reports, 15, 638-650.
• Castillo-Quan, J.I., Kinghorn, K.J., and Bjedov, I. (2015). Genetics and pharmacology of longevity: The road to therapeutics for healthy aging. Advances in Genetics, 90, 1–101.
• Additional publications can be found on Google Scholar, ORCID, or NCBI bibliography.

Selected Honors, Research Support and Professional Activities

• Early Career Scholar, American Aging Association (AGE), 2026.
• Member of the International Consortium to Classify Ageing-related pathologies (ICCARP).
• Glenn Foundation for Medical Research Postdoctoral Fellowship in Aging Research, American Federation for Aging Research.

Current Research Themes

The CORA Laboratory is actively recruiting Ph.D. students for direct admission beginning Fall 2027.

• Lipid signaling and longevity
  • How do specific lipid species and changes in lipid metabolism communicate with cellular stress-response pathways to influence aging?
• ER–lipid droplet biology and proteostasis
  • How does communication between the endoplasmic reticulum and lipid droplets regulate protein quality control, ER-associated degradation, and metabolic resilience?
• Protein folding and metabolic adaptation
  • How is protein-folding capacity coordinated with cellular metabolic states, and how do changes in cytosolic and endoplasmic reticulum proteostasis shape adaptive stress responses and organismal resilience?
• SKN-1/Nrf biology
  • How are SKN-1/Nrf transcription factors activated by metabolic, oxidative, and proteotoxic stress, and how do their transcriptional programs promote cellular and organismal homeostasis?
• Mechanisms of resilience during aging
  • Why are some cells and organisms better able to tolerate metabolic and environmental stress, and can these resilience mechanisms reveal fundamental principles of healthy aging?