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Draft:Maria Hatzoglou

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  • Comment: In accordance with the Wikimedia Foundation's Terms of Use, I disclose that I have been paid by my employer for my contributions to this article. HRShami (talk) 05:30, 30 July 2026 (UTC)
Maria Hatzoglou
EducationUniversity of Thessaloniki, B.S.
University of Athens, Ph.D.
Known forResearch on Endoplasmic reticulum stress response; integrated stress response; translational control
Scientific career
FieldsMolecular biology; cell biology; translational control
InstitutionsCase Western Reserve University

Maria Hatzoglou is a molecular biologist and professor in the Department of Genetics and Genome Sciences at the Case Western Reserve University School of Medicine. Her research work has focused on the cellular stress response, particularly endoplasmic reticulum (ER) stress, the integrated stress response (ISR), and the translational control of gene expression and its implications for cancer, diabetes, and neurodegenerative disease.

Education

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Hatzoglou received a degree in chemistry from the University of Thessaloniki in 1981. She completed her Ph.D. at the University of Athens in 1985, working on the structure and function of heterogeneous nuclear ribonucleoproteins and on RNA splicing.[1] She subsequently undertook postdoctoral training in the Department of Biochemistry at Case Western Reserve University, studying the regulation of gene expression of retrovirus-borne genes following infection of cells.[1][2]

Career

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Hatzoglou joined the faculty of the Department of Nutrition at Case Western Reserve University in 1991.[1] She is a professor in the Department of Genetics and Genome Sciences at the School of Medicine and holds an appointment in nutrition,[3][4] and is affiliated with the Center for RNA Science and Therapeutics.[5] She is a member of the Molecular Oncology Program at the Case Comprehensive Cancer Center.[6]

Research

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Hatzoglou's group has characterized mechanisms of translational control[7] and metabolic regulation during cellular stress.[8] She co-authored studies of how ISR adaptive pathways are exploited by cancer cells[9] to support metastasis[10] and tumor growth.[11] Additionally, she described how chronic ER stress can increase protein synthesis in a manner that contributes to cell death.[12]

Hatzoglou has worked on the regulation of amino acid transport[13] and cellular adaptation to osmotic stress.[14] Her work has examined the regulation of the neutral amino acid transporter SNAT2[13] and the phosphatase regulatory subunit GADD34 in adaptation to increased extracellular osmolarity.[14] She described an osmoadaptation mechanism in which coordinated regulation of GADD34 and the amino acid transporter SNAT2 enables cellular adaptation to increased extracellular osmolarity.[15] In 2011, she received an NIH R37 Award for her project "Translational Control by Osmotically Active Solutes".[16]

In 2025, Hatzoglou authored a study in Nature describing the "split integrated stress response" (s-ISR),[17] in which she and her collaborators reported that ISR signaling exhibits substantial plasticity rather than functioning as a linear binary switch.[18] She further added that the integrated stress response can be fine-tuned according to the nature, intensity, and duration of stress. The work used mouse models of vanishing white matter disease and suggested that similar stress-adaptation mechanisms may operate in other neurodegenerative disorders, including multiple sclerosis and amyotrophic lateral sclerosis.[19]

In a series of papers, Hatzoglou participated as a collaborator in studies that presented translational reprogramming as a driver of cancer cell plasticity. A 2020 study linked selective mRNA translation under hypoxic conditions to increased breast cancer cell plasticity, thereby promoting cellular state transitions associated with metastasis and reduced treatment sensitivity.[20] In 2021, she reported that the integrated stress response is a key driver of KRAS-driven lung tumorigenesis[21] and that inhibiting it substantially reduced tumor growth.[11] As a lead author of the study, she showed that insulin-producing β-cells can lose and subsequently regain their mature identity in response to chronic ER stress following stress relief, with implications for the progression of type 1 diabetes.[22]

References

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  1. 1 2 3 "Maria Hatzoglou, Ph.D." Department of Pharmacology, Case Western Reserve University. Archived from the original on 19 January 2019. Retrieved 30 July 2026.
  2. ↑ "5 questions with…Case Medal for Excellence in Health Science Innovation winner Maria Hatzoglou". Case Western Reserve University School of Medicine. 5 November 2021. Retrieved 30 July 2026.
  3. ↑ "Maria Hatzoglou, PhD". Case Western Reserve University. 25 April 2025. Retrieved 1 July 2026.
  4. ↑ "Two Studies Find Stress Reprograms Cells". Case Western Reserve University School of Medicine. 15 November 2018. Retrieved 30 July 2026.
  5. ↑ "Maria Hatzoglou, PhD". Center for RNA Science and Therapeutics, Case Western Reserve University. 25 April 2025. Retrieved 30 July 2026.
  6. ↑ "Maria Hatzoglou, PhD". Case Comprehensive Cancer Center, Case Western Reserve University. 25 April 2025. Retrieved 30 July 2026.
  7. ↑ Shin, Sejeong; Han, Min-Joon; Jedrychowski, Mark P.; Zhang, Ziyang; Shokat, Kevan M.; Plas, David R.; Dephoure, Noah; Yoon, Sang-Oh (2023). "mTOR inhibition reprograms cellular proteostasis by regulating eIF3D-mediated selective mRNA translation and promotes cell phenotype switching". Cell Reports. 42 (8): 14. doi:10.1016/j.celrep.2023.112868. PMC 10528759. PMID 37494188.
  8. ↑ Li, Xiaolu; Zhang, Tong; Day, Nicholas J.; Feng, Song; Gaffrey, Matthew J.; Qian, Wei-Jun (2022). "Defining the S-Glutathionylation Proteome by Biochemical and Mass Spectrometric Approaches". Antioxidants. 11 (11): 12. doi:10.3390/antiox11112272. PMID 36421458.
  9. ↑ Zhang, Guangyu; Wang, Xiaoding; Rothermel, Beverly A.; Lavandero, Sergio; Wang, Zhao V. (2022). "The integrated stress response in ischemic diseases". Cell Death and Differentiation. 29 (4): 754. doi:10.1038/s41418-021-00889-7. PMC 8990009. PMID 34743204.
  10. ↑ Chen, Siyu; Navickas, Albertas; Goodarzi, Hani (2024). "Translational adaptation in breast cancer metastasis and emerging therapeutic opportunities". Trends in Pharmacological Sciences. 45 (4): 315. doi:10.1016/j.tips.2024.02.002. PMID 38453522.
  11. 1 2 Lu, Hao-Jun; Koju, Nirmala; Sheng, Rui (2024). "Mammalian integrated stress responses in stressed organelles and their functions". Acta Pharmacologica Sinica. 45 (6): 1106. doi:10.1038/s41401-023-01225-0. ISSN 1745-7254. PMC 11130345. PMID 38267546.
  12. ↑ Grootjans, Joep; Kaser, Arthur; Kaufman, Randal J.; Blumberg, Richard S. (2016). "The unfolded protein response in immunity and inflammation". Nature Reviews. Immunology. 16 (8): 469–484. Bibcode:2016NatRI..16..469G. doi:10.1038/nri.2016.62. PMC 5310224. PMID 27346803.
  13. 1 2 Spriggs, Keith A.; Bushell, Martin; Willis, Anne E. (2010). "Translational regulation of gene expression during conditions of cell stress". Molecular Cell. 40 (2): 231. doi:10.1016/j.molcel.2010.09.028. PMID 20965418.
  14. 1 2 Guindolet, Damien; Woodward, Ashley M.; Gabison, Eric E.; Argüeso, Pablo (2022). "Alleviation of Endoplasmic Reticulum Stress Enhances Human Corneal Epithelial Cell Viability under Hyperosmotic Conditions". International Journal of Molecular Sciences. 23 (9): 8. doi:10.3390/ijms23094528. PMC 9104051. PMID 35562919.
  15. ↑ Menchini, Robin Johansen; Chaudhry, Farrukh Abbas (2019). "Multifaceted regulation of the system A transporter Slc38a2 suggests nanoscale regulation of amino acid metabolism and cellular signaling". Neuropharmacology. 161 107789: 5. doi:10.1016/j.neuropharm.2019.107789. PMID 31574264.
  16. ↑ "Translational Control by Osmotically Active Solutes". NIH Research Portfolio Online Reporting Tools (RePORT). Retrieved July 9, 2026.
  17. ↑ Erb, Anthony L.; Young-Baird, Sara K. (2026). "CDC123 is an ATPase that modulates mRNA translation and the integrated stress response by regulating eIF2 complex assembly". The Journal of Biological Chemistry. 302 (2): 8. doi:10.1016/j.jbc.2025.111116. PMC 12860950. PMID 41461316.
  18. ↑ Park, Moon Nyeo (2026). "Therapy as a State-Generator: Dynamic Phenotypic Landscapes and Adaptive Stress Circuits in Chemotherapy Resistance of Breast Cancer". Antioxidants. 15 (4): 4. doi:10.3390/antiox15040459. PMC 13113182. PMID 42072101.
  19. ↑ "How Cells Respond to Stress Is More Nuanced than Previously Believed".
  20. ↑ Amiri, Mehdi; Mahmood, Niaz; Tahmasebi, Soroush; Sonenberg, Nahum (2025). "eIF4F-mediated dysregulation of mRNA translation in cancer". RNA (New York, N.Y.). 31 (3): 418. doi:10.1261/rna.080340.124. PMC 11874970. PMID 39809544.
  21. ↑ Su, Hang; Chen, Li; Wu, Jun; Cheng, Zhongyi; Li, Jing; Ren, Yijiu; Xu, Junfang; Dang, Yifang; et al. (2025). "Proteogenomic characterization reveals tumorigenesis and progression of lung cancer manifested as subsolid nodules". Nature Communications. 16 (1): 11. Bibcode:2025NatCo..16.2414S. doi:10.1038/s41467-025-57364-x. PMID 40069142.
  22. ↑ Sahin, Gulcan Semra; Lee, Hugo; Engin, Feyza (2021). "An accomplice more than a mere victim: The impact of β-cell ER stress on type 1 diabetes pathogenesis". Molecular Metabolism. 54 101365: 7. doi:10.1016/j.molmet.2021.101365. PMC 8606542. PMID 34728341.
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