Biography:Fabiola Terzi

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Short description: Italian-French scientist and physician

Fabiola Terzi (born January 9, 1961 in Seriate, Bergamo, Italy) is an Italian-French scientist and physician. She is known for her research on chronic kidney disease. Since January 2020, she serves as the director of the research Institut Necker-Enfants Malades (INEM) in Paris.[1]

Life and career

Terzi attended medical school at the University of Milan where she graduated with a medical degree (M.D.) in 1986.[2][3] She then trained as a pediatrician in the team of Professor Fabio Sereni in Milan specializing in pediatric nephrology.[2][3] In 1989 she moved to Paris where she worked on a Ph.D. project under the supervision of Professor Claire Kleinknecht (Necker-Enfants Malades Hospital, Paris) developing her interest for the molecular mechanisms of renal diseases.[2][3][4][5] After her doctorate, Terzi went on to train as a postdoc in the team of Professor Pascal Briand (Institut Cochin, Paris).[2][3][6][7] She holds an HDR degree (French for: Habilitation à Diriger des Recherches; English: Accreditation to Direct Research), the highest academic degree to be awarded in France.[8]

With time she progressively focused on the physiopathology of chronic kidney disease (CKD). From 2003 on, Terzi began to build up her own laboratory ("Mechanisms and Therapeutic Strategies of Chronic Kidney Disease"), which she has headed since then.[2][3] Upon the founding of the Institute Necker-Enfants Malades (INEM) in 2014, a research center affiliated to the French National Institute of Health and Medical Research, the French National Center for Scientific Research and to the University of Paris, Terzi became head of its “Growth and Signaling” department.[2][3] Since January 2020, she serves as the director of INEM responsible for 19 research teams (as of October 2021).[1][3] Besides, she is editor of the “Experimental Nephrology and Genetics” section of the journal Nephron since 2015.[9]

Scientific contribution

Terzi’s scientific work centers on the cellular events contributing either to the prevention or progression of chronic kidney disease (CKD) and on characterizing the pathways and genetic programs underlying these events.[10] She developed distinct experimental models of CKD, above all a model of nephron reduction, leading her to the discovery of pathways and potential pharmacological targets driving CKD.[11][12][13] In particular, Terzi’s Team revealed a detrimental role of the epidermal growth factor receptor (EGFR) pathway in the fate of CKD, the activation of which aggravates renal lesions after nephron reduction.[14][15]

Beyond that, Terzi has been involved in several translational studies that have succeeded in the identification of novel biomarkers (of the progression) of renal diseases in humans. The latter are protected by four patent filings (as of October 2021).[3]

Along with other world-renowned CKD experts, she is co-initiator of TrainCKDis, a European training programme intended to prepare the next generation of top-level CKD scientists funded by the European Union’s Horizon 2020 research and innovation programme.[16]

Awards and honors

For her scientific contributions to the field of nephrology she has been awarded the Grand Prize of the French National Academy of Medicine (French: Grand Prix de l’Académie Nationale de Médecine) in 2009 and the Prize of the French Kidney Foundation (French: Prix de la Fondation du Rein) in 2011.[3][17][18]

References

  1. ↑ 1.0 1.1 "Institut Necker Enfants Malades". https://www.institut-necker-enfants-malades.fr/index.php?menu=team&lang=en. 
  2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 "Institut Necker Enfants Malades". https://www.institut-necker-enfants-malades.fr/index.php?menu=team&rubric=teamtabs&idfac=terzi&lang=en#biosketch. 
  3. ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 3.8 "Université de Paris | TrainCKDis". https://www.trainckdis.eu/consortium/beneficiaries/universite-de-paris. 
  4. ↑ Terzi, F. et al. (May 1995). "Subtotal but not unilateral nephrectomy induces hyperplasia and protooncogene expression". The American Journal of Physiology 268 (5 Pt 2): F793–801. doi:10.1152/ajprenal.1995.268.5.F793. ISSN 0002-9513. PMID 7539585. https://pubmed.ncbi.nlm.nih.gov/7539585. 
  5. ↑ Kleinknecht, C. et al. (June 1995). "Experimental models of nephron reduction: some answers, many questions". Kidney International. Supplement 49: S51–54. ISSN 0098-6577. PMID 7674595. https://pubmed.ncbi.nlm.nih.gov/7674595. 
  6. ↑ Terzi, F. et al. (April 1997). "Normal tubular regeneration and differentiation of the post-ischemic kidney in mice lacking vimentin". The American Journal of Pathology 150 (4): 1361–1371. ISSN 0002-9440. PMID 9094992. PMC 1858176. https://pubmed.ncbi.nlm.nih.gov/9094992. 
  7. ↑ Terzi, F. et al. (September 1997). "Reduction of renal mass is lethal in mice lacking vimentin. Role of endothelin-nitric oxide imbalance". The Journal of Clinical Investigation 100 (6): 1520–1528. doi:10.1172/JCI119675. ISSN 0021-9738. PMID 9294120. PMC 508333. https://pubmed.ncbi.nlm.nih.gov/9294120. 
  8. ↑ "Mécanismes et stratégies thérapeutiques des maladies rénales chroniques / Liste des équipes d'accueil / Equipes de recherche / ed157 / La Formation doctorale à l'Université Paris Descartes - ed157". https://ecolesdoctorales.parisdescartes.fr/ed157/Equipes-de-recherche/Liste-des-equipes-d-accueil/Mecanismes-et-strategies-therapeutiques-des-maladies-renales-chroniques. 
  9. ↑ (in en) Nephron | Karger Journal. https://www.karger.com/Journal/Home/223854. 
  10. ↑ "Institut Necker Enfants Malades". https://www.institut-necker-enfants-malades.fr/index.php?menu=team&rubric=teamtabs&idfac=terzi&lang=en. 
  11. ↑ Canaud, Guillaume et al. (October 2013). "AKT2 is essential to maintain podocyte viability and function during chronic kidney disease". Nature Medicine 19 (10): 1288–1296. doi:10.1038/nm.3313. ISSN 1546-170X. PMID 24056770. https://pubmed.ncbi.nlm.nih.gov/24056770. 
  12. ↑ El Karoui, Khalil et al. (April 2016). "Endoplasmic reticulum stress drives proteinuria-induced kidney lesions via Lipocalin 2" (in en). Nature Communications 7 (1): 10330. doi:10.1038/ncomms10330. ISSN 2041-1723. PMID 26787103. Bibcode: 2016NatCo...710330E. 
  13. ↑ Zaidan, Mohamad et al. (July 2020). "Signaling pathways predisposing to chronic kidney disease progression" (in en). JCI Insight 5 (9): e126183. doi:10.1172/jci.insight.126183. ISSN 2379-3708. PMID 32376805. PMC 7253021. https://insight.jci.org/articles/view/126183. 
  14. ↑ Terzi, F. et al. (July 2000). "Targeted expression of a dominant-negative EGF-R in the kidney reduces tubulo-interstitial lesions after renal injury". The Journal of Clinical Investigation 106 (2): 225–234. doi:10.1172/JCI8315. ISSN 0021-9738. PMID 10903338. PMC 314303. https://pubmed.ncbi.nlm.nih.gov/10903338. 
  15. ↑ Lautrette, Alexandre et al. (August 2005). "Angiotensin II and EGF receptor cross-talk in chronic kidney diseases: a new therapeutic approach" (in en). Nature Medicine 11 (8): 867–874. doi:10.1038/nm1275. ISSN 1078-8956. PMID 16041383. http://www.nature.com/articles/nm1275. 
  16. ↑ "TrainCKDis | TrainCKDis". https://www.trainckdis.eu/trainckdis. 
  17. ↑ "Lauréats 2009 – Académie nationale de médecine | Une institution dans son temps" (in fr-FR). https://www.academie-medecine.fr/laureats-2009/. 
  18. ↑ "Prix de la Fondation du Rein – Fondation du rein" (in fr-FR). https://www.fondation-du-rein.org/prix-de-la-fondation-du-rein/. 

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