Thibaut Quillard, Laurent Beck, Sarah Beck-Cormier, Blandine Maurel

Atherosclerosis and its complications remain the main cause of death worldwide. The clinical outcomes of atherosclerotic lesions (myocardial infarcts, stroke, acute ischemia of the limbs…) directly depend on their composition.
  • In our group, we aim to better understand the physiopathology of atherosclerotic plaques formation and development. Atherosclerotic plaques can present various compositions. Such differences are often found between arterial beds, notably with carotid arteries developing typically lipid-rich and inflamed lesions, while femoral arteries mostly associate with fibrous and heavily calcified lesions. Because vascular cells (endothelial and smooth muscle cells) from these anatomical locations have specific transcriptomic signatures and identities, we will investigate how cardiovascular risk factor affect carotid and femoral vascular cell phenotypes and responses, and how this further translates into differential plaque development. Identification of molecular determinants implicated in these responses will help better understand atherosclerosis development, and will provide with novel therapeutic strategies based on lesion composition and localization. Our work will also study how hemodynamics impacts vascular cells phenotype, as carotid and femoral arteries are also exposed to specific blood flow dynamics. (T. Quillard, B. Maurel)
  • Calcification of atherosclerotic lesions is an independent predictive factor for cardiovascular complications and death, by affecting locally plaque stability, thrombus formation, endovascular treatment success, and more globally by greatly impacting vascular rigidity and vascular blood system resistance. In chronic kidney disease, hyperphosphatemia triggers calcification of the arterial wall which contribute to the developmentnt of cardiovascular diseases. There is still no treatment targeting this pathological process of vascular calcification in those two diseases, partly because the mechanisms underlying their formation and development are still poorly characterized. Thanks to our human biocollection of human atherosclerotic lesions and healthy arteries, and novel murine experimental models, we aim to identify new molecular players regulating this process and better understand the role(s) of the PiT1/SLC20A1 and PiT2/SLC20A2 proteins. (L. Beck, S. Beck-Cormier). These two proteins are at the cross-road of mineralization and metabolism, a role that we previously illustrated in investigating the relationship between skeleton, bone vessels and bone marrow adiposity. Deeper analysis of their involvement in adipose tissue (energy metabolism and thermogenesis) in currently ongoing through a collaboration with Xavier Prieur (team IV) (S. Beck-Cormier, L. Beck).


PiT2 deficiency prevents increase of bone marrow adipose tissue during skeletal maturation but not in OVX-induced osteoporosis. Frangi G, Guicheteau M, Jacquot F, Pyka G, Kerckhofs G, Feyeux M, Veziers J, Guihard P, Halgand B, Sourice S, Guicheux J, Prieur X, Beck L, Beck-Cormier S. Front Endocrinol (Lausanne). 2022 Nov 16;13:921073. doi: 10.3389/fendo.2022.921073. eCollection 2022. PMID: 36465661 Free PMC article.

Distinct role of mitochondrial function and protein kinase C in intimal and medial calcification in vitro. Heuschkel MA, Babler A, Heyn J, van der Vorst EPC, Steenman M, Gesper M, Kappel BA, Magne D, Gouëffic Y, Kramann R, Jahnen-Dechent W, Marx N, Quillard T, Goettsch C. Front Cardiovasc Med. 2022 Sep 20;9:959457. doi: 10.3389/fcvm.2022.959457. eCollection 2022. PMID: 36204585 Free PMC article.
PiT1/Slc20a1 Is Required for Endoplasmic Reticulum Homeostasis, Chondrocyte Survival, and Skeletal Development. Couasnay G, Bon N, Devignes CS, Sourice S, Bianchi A, Véziers J, Weiss P, Elefteriou F, Provot S, Guicheux J, Beck-Cormier S, Beck L. J Bone Miner Res. 2019 Feb;34(2):387-398. doi: 10.1002/jbmr.3609. Epub 2018 Nov 20.
The Need of a Paradigm Shift to Better Understand PiT1 and PiT2 Biology: Response to "Why Is There No PiT1/SLC20A1 Pathogenic Variants Yet Linked to Primary Familial Brain Calcification?". Beck-Cormier S, Beck L. J Bone Miner Res. 2020 Apr;35(4):825-826. doi: 10.1002/jbmr.3969. Epub 2020 Feb 12. PMID: 32049372 Free article. No abstract available.
Slc20a2, Encoding the Phosphate Transporter PiT2, Is an Important Genetic Determinant of Bone Quality and Strength. Beck-Cormier S, Lelliott CJ, Logan JG, Lafont DT, Merametdjian L, Leitch VD, Butterfield NC, Protheroe HJ, Croucher PI, Baldock PA, Gaultier-Lintia A, Maugars Y, Nicolas G, Banse C, Normant S, Magne N, Gérardin E, Bon N, Sourice S, Guicheux J, Beck L, Williams GR, Bassett JHD, J Bone Miner Res. 2019 Jun;34(6):1101-1114. doi: 10.1002/jbmr.3691. Epub 2019 Mar 19. PMID: 30721528 Free PMC article.

Inhibition of alkaline phosphatase impairs dyslipidemia and protects mice from atherosclerosis. Bessueille L, Kawtharany L, Quillard T, Goettsch C, Briolay A, Taraconat N, Balayssac S, Gilard V, Mebarek S, Peyruchaud O, Duboeuf F, Bouillot C, Pinkerton A, Mechtouff L, Buchet R, Hamade E, Zibara K, Fonta C, Canet-Soulas E, Millan JL, Magne D.
Transl Res. 2023 Jan;251:2-13. doi: 10.1016/j.trsl.2022.06.010. Epub 2022 Jun 17.



  • ANR
  • Fondation de l'Avenir
  • Fondation Maladie Rare
  • Genavie
  • Région Pays de la Loire
  • Société française de cardiologie
  • Société Francophone du Diabète
  • Société Française de Rhumatologie
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