Pilar Alcaide is a Spanish-born cardiac biologist and immunologist at the Tufts University School of Medicine. She is Kenneth and JoAnn G. Wellner Professor and Assistant Dean of Faculty Development.[1]
Pilar Alcaide | |
|---|---|
| Born | |
| Alma mater | Universidad Autonoma de Madrid, Spain (MS, PhD) |
| Scientific career | |
| Fields | Cardiovascular biology, immunology |
| Institutions | Tufts University School of Medicine |
| Website | https://gsbs.tufts.edu/faculty-research/pilar-alcaide-lab |
Life and Career
editAlcaide spent her early life in Madrid, Spain, though was born in Guadalajara. She remained in Madrid for college and graduate school, completing an M.S. from the Universidad Autonoma de Madrid in 1998, and received her PhD from the same institution in 2003.[2][1]
Dr. Alcaide then undertook postdoctoral research at Brigham and Women's Hospital and Harvard Medical School as part of a Fulbright scholarship. She continued her research at Harvard Medical School as an Instructor of Pathology, having been awarded an NIH K99 Pathway to Independence grant.[3] In 2011, she joined the faculty of the Tufts University School of Medicine as an assistant professor. Alcaide was promoted to associate professor in 2016, full professor in 2023, and in 2019 was also named to the Kenneth and JoAnn G. Wellner professorship. Since 2020 she has served as Program Director of the Tufts University Graduate School of Biomedical Science immunology program, and since 2021 has been Assistant Dean of Faculty Development.[1]
Research
editAlcaide's lab researches interactions between the immune and cardiovascular systems, with particular focuses on cardiac T-cells and the immune response to heart failure.[4][5]
One recent project from Alcaide's group examined how T-cell recruitment to the heart following heart failure affected the progression of heart failure pathogenesis. They found that a specific population of T-cells responds to the heart following nonischemic heart failure, and that these immune cells drive cardiac fibrosis, in turn negatively affecting heart function following injury.[6][7][8]
Another research area that Alcaide's lab is investigating is how the immune response to doxorubicin, a common chemotherapy drug, can lead to negative cardiac outcomes (heart failure and/or cardiomyopathy). A collaboration with Junjie Xiao's research group found exercise protected against cardiotoxicity by affecting B-cell activation.[9][10] Separately, Alcaide's group found that CD8+ T cells drive cardiac inflammation following doxorubicin treatment which leads to cardiac fibrosis and other negative outcomes.[11][12]
Honors and awards
edit- ASIP Cotran Early Career Investigator Award[citation needed]
- Fellow of the American Heart Association[citation needed]
References
edit- ^ a b c "Pilar Alcaide | Faculty Profile". facultyprofiles.tufts.edu. Retrieved 2024-08-10.
- ^ Todorovic, Vesna (2023-03-13). "In conversation with Pilar Alcaide". Nature Cardiovascular Research. 2 (3): 208–209. doi:10.1038/s44161-023-00240-y. ISSN 2731-0590.
- ^ "Pilar Alcaide, PhD". American Society for Investigative Pathology. Retrieved 2024-08-11.
- ^ "'El problema de la ciencia en España es la endogamia' | Biociencia | elmundo.es". www.elmundo.es. Retrieved 2024-08-13.
- ^ "The Pilar Alcaide Lab | Graduate School of Biomedical Sciences". gsbs.tufts.edu. Retrieved 2024-08-13.
- ^ Nevers, Tania; Salvador, Ane M.; Grodecki-Pena, Anna; Knapp, Andrew; Velázquez, Francisco; Aronovitz, Mark; Kapur, Navin K.; Karas, Richard H.; Blanton, Robert M.; Alcaide, Pilar (2015-05-28). "Left Ventricular T-Cell Recruitment Contributes to the Pathogenesis of Heart Failure". Circulation: Heart Failure. 8 (4): 776–787. doi:10.1161/CIRCHEARTFAILURE.115.002225. ISSN 1941-3289. PMC 4512916. PMID 26022677.
- ^ Nevers, Tania; Salvador, Ane M.; Velazquez, Francisco; Ngwenyama, Njabulo; Carrillo-Salinas, Francisco J.; Aronovitz, Mark; Blanton, Robert M.; Alcaide, Pilar (2017-11-06). "Th1 effector T cells selectively orchestrate cardiac fibrosis in nonischemic heart failure". Journal of Experimental Medicine. 214 (11): 3311–3329. doi:10.1084/jem.20161791. ISSN 0022-1007. PMC 5679176. PMID 28970239.
- ^ "Uncovering a Link Between Inflammation and Heart Disease | Tufts Now". now.tufts.edu. 2021-02-01. Retrieved 2024-08-13.
- ^ Wang, Jing; Liu, Shuqin; Meng, Xinxiu; Zhao, Xuan; Wang, Tianhui; Lei, Zhiyong; Lehmann, H. Immo; Li, Guoping; Alcaide, Pilar; Bei, Yihua; Xiao, Junjie (2024-02-07). "Exercise Inhibits Doxorubicin-Induced Cardiotoxicity via Regulating B Cells". Circulation Research. 134 (5): 550–568. doi:10.1161/CIRCRESAHA.123.323346. ISSN 0009-7330. PMC 11233173. PMID 38323433.
- ^ Gutierrez, Alan; Moslehi, Javid J. (2024-02-29). "B-Cell Immune Checkpoints Come of Age in Cardio-oncology". Circulation Research. 134 (5): 569–571. doi:10.1161/CIRCRESAHA.124.324243. ISSN 0009-7330. PMC 11141201. PMID 38422182.
- ^ Bayer, Abraham L.; Zambrano, Maria A.; Smolgovsky, Sasha; Robbe, Zachary L.; Ariza, Abul; Kaur, Kuljeet; Sawden, Machlan; Avery, Anne; London, Cheryl; Asnani, Aarti; Alcaide, Pilar (2024-07-17). "Cytotoxic T cells drive doxorubicin-induced cardiac fibrosis and systolic dysfunction". Nature Cardiovascular Research: 1–17. doi:10.1038/s44161-024-00507-y. ISSN 2731-0590.
- ^ Sattler, Susanne; Ljubojevic-Holzer, Senka (2024-07-17). "CD8+ T cells as the missing link between doxorubicin cancer therapy and heart failure risk". Nature Cardiovascular Research: 1–3. doi:10.1038/s44161-024-00513-0. ISSN 2731-0590.