Dr. Lopez-Ramirez

Dr. Miguel Alejandro Lopez-Ramirez is focused on the development of non-invasive drug treatments to treat cardiovascular and neurological diseases. 

Dr. Lopez-Ramirez received degrees in Pharmaceutical Science and in Molecular and Cellular Neurobiology. He is trained as a Neurovascular Biologist researching the molecular and genetic mechanisms that provide understanding of the pathological and physiological roles of genetic abnormalities. He received postdoctoral research training studying vascular network formation in living organisms at Yale University. He then moved to UCSD to study the roles of genes involved in cerebral cavernous malformations and their implications in cardiovascular biology.  Dr. Lopez-Ramirez is now an Assistant Professor in the School of Medicine at UC San Diego. 

About the Lab

Our lab uses integrated approaches including genetics, cell biology, and bioinformatic tools to increase our understanding of the biological components of cerebral cavernous malformations (CCMs) and neuroinflammation. CCMs are brain vascular malformations prone to repetitive hemorrhagic stroke, which cause neurological deficit and occasionally death in ~0.5% of the population. Currently no pharmacological therapy exists for those afflicted. Our research has demonstrated that mild angiogenesis inhibitors including thrombospondin1 derivatives may provide a novel opportunity to treat CCMs. In addition, our research has pioneered the important role of endothelial microRNAs as regulators of cerebrovascular integrity during health and neuroinflammation. The ultimate goal of our research is to provide non-invasive, safe, and effective therapies to cardiovascular and neurological diseases.

Research Highlights

Recent Publications

  • Neuroinflammation plays a critical role in cerebral cavernous malformation disease. Catherine Chinhchu Lai*, Bliss Nelsen*, Eduardo Frias-Anaya*, Helios Gallegos-Gutierrez*, Marco Orecchioni, Hao Sun,  Klaus Ley, Brendan Gongol, Miguel A. Lopez-Ramirez. *contributed equally. BioRxiv, 2022.2005.2009.491214 (2022).

  • Astrocytes propel neurovascular dysfunction during cerebral cavernous malformation lesion formation. M. A. Lopez-Ramirez, S. I. Soliman, P. Hale, C. C. Lai, A. Pham, E. Estrada, S. McCurdy, R. Girard, R. Verma, T. Moore, R. Lightle, N. Hobson, R. Shenkar, O. Poulsen, G. G. Haddad, R. Daneman, B. Gongol, H. Sun, F. Lagarrigue, I.A. Awad, M. H. Ginsberg. Journal of Clinical Investigation, 2021.

  • Inhibition of the HEG1-KRIT1 interaction increases KLF4 and KLF2 expression in endothelial cells. M.A. Lopez-Ramirez, Mark K. Haynes, Preston Hale, Killian Oukoloff, Matthew Bautista, Brendan Gongol, John Y. Shyy, Carlo Ballatore, Larry A. Sklar, Alexandre R. Gingras. FASEB BioAdvances, 2021.

  • Distinct integrin activation pathway for effector and regulatory T cell trafficking and function. Sun H., Lagarrigue F, Wang H, Fan Z., Lopez-Ramirez MA, Chang JT, Ginsberg M.H. Journal of Experimental Medicine. 2021.

  • Generation of in vitro models of Cerebral Cavernous Malformations disease. Hale P., Soliman S.I., Lopez-Ramirez MA. Springer Nature. Methods Mol Biol. 2020.