Fabiola Terzi 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]
Fabiola Terzi | |
|---|---|
| Citizenship | Italian, French |
| Education | University of Milan, University of Paris 7 |
| Known for | Studies of the physiopathology of chronic kidney disease |
| Awards | Grand Prize of the Académie Nationale de Médecine, Prize of the French Kidney Foundation |
| Scientific career | |
| Fields | Paediatrics |
Life and career
editFabiola 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 continued her specialization in pediatric nephrology in the team of Professor Michael Broyer and started a Ph.D. project under the supervision of Professor Claire Kleinknecht (Université Paris Diderot, Paris) developing her interest for the molecular mechanisms of renal diseases.[2][3][4][5] After her doctorate, she went on to train as a postdoc, first in the team of Professor Pascal Briand (Institut Cochin, Paris), then in the team of Professor Gérard Friedlander (Faculté de Médecine, Site Bichat, Paris).[2][3][6][7]
With time she progressively focused on the physiopathology of chronic kidney disease (CKD). From 2003 on, she 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, she became head of the “Growth and Signaling” department.[2][3] Since January 2020, she serves as the director of INEM responsible for 19 research teams (as of July 2022).[1][3] Besides, she is editor of the “Experimental Nephrology and Genetics” section of the journal Nephron since 2015.[8]
Scientific contribution
editFabiola 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.[9] 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.[10][11][12] In particular, her 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.[13][14]
Beyond that, she has been involved in several translational studies that have succeeded in the identification of novel biomarkers (of the progression) of renal diseases in humans. These latter are protected by five patent filings (as of July 2022).[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.[15]
Awards and honors
editFor 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][16][17]
References
edit- ^ a b "Institut Necker Enfants Malades". www.institut-necker-enfants-malades.fr. Retrieved 2021-05-15.
- ^ a b c d e f "Institut Necker Enfants Malades". www.institut-necker-enfants-malades.fr. Retrieved 2021-05-15.
- ^ a b c d e f g h i "Université de Paris | TrainCKDis". www.trainckdis.eu. Retrieved 2021-05-15.
- ^ 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.
- ^ 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.
- ^ 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. PMC 1858176. PMID 9094992.
- ^ 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. PMC 508333. PMID 9294120.
- ^ "Nephron | Karger Journal".
{{cite journal}}: Cite journal requires|journal=(help) - ^ "Institut Necker Enfants Malades". www.institut-necker-enfants-malades.fr. Retrieved 2021-05-15.
- ^ 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. S2CID 24844397.
- ^ El Karoui, Khalil; et al. (April 2016). "Endoplasmic reticulum stress drives proteinuria-induced kidney lesions via Lipocalin 2". Nature Communications. 7 (1): 10330. Bibcode:2016NatCo...710330E. doi:10.1038/ncomms10330. ISSN 2041-1723. PMC 4735759. PMID 26787103.
- ^ Zaidan, Mohamad; et al. (July 2020). "Signaling pathways predisposing to chronic kidney disease progression". JCI Insight. 5 (9): e126183. doi:10.1172/jci.insight.126183. ISSN 2379-3708. PMC 7253021. PMID 32376805.
- ^ 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. PMC 314303. PMID 10903338.
- ^ Lautrette, Alexandre; et al. (August 2005). "Angiotensin II and EGF receptor cross-talk in chronic kidney diseases: a new therapeutic approach". Nature Medicine. 11 (8): 867–874. doi:10.1038/nm1275. ISSN 1078-8956. PMID 16041383. S2CID 7909149.
- ^ "TrainCKDis | TrainCKDis". www.trainckdis.eu. Retrieved 2021-05-16.
- ^ "Lauréats 2009 – Académie nationale de médecine | Une institution dans son temps" (in French). Retrieved 2021-01-16.
- ^ "Prix de la Fondation du Rein – Fondation du rein" (in French). Retrieved 2021-01-16.