Cristina Espinosa-Diez, PhD
May 31, 2024
Assistant Professor
Wayne State University
Primary Research:
Welcome to the Espinosa-Diez lab, where we are dedicated to understanding how external stressors impact vascular remodeling and dysfunction. Our research primarily explores the impact of cancer therapeutics and DNA-damaging agents on vascular health, particularly through changes in epigenetic modifications like DNA methylation and the behavior of non-coding RNAs. We are currently excited about our work with two promising lncRNA candidates. The first plays a key role in maladaptive stress responses in vascular endothelial cells, with its absence leading to increased cell death and reduced angiogenesis. The second lncRNA is repressed in response to increased Angiotensin-II, and its loss leads to vascular hypertrophy and senescence, playing a significant role in vascular remodeling. Supported by AHA funding, we are exploring its role in microvascular alterations and its contribution to the progression of kidney disease. Beyond research, our lab is deeply committed to mentoring the next generation of scientists, fostering a diverse and inclusive environment, and emphasizing the power of teamwork in driving scientific discovery. Stay tuned for more novel lncRNA candidates from our lab!
Laboratory web site URL:
https://www.espinosadiezlab.com/
Recent Presentations:
- Linc(RNA)s to microvascular disease. Hypertension and Vascular Division Research Seminars, Henry Ford Foundation; Detroit, MI, United States of America. 03/2024.
- Role of ncRNAs Controlling Vascular Cell Fate in Response to Cellular Stress. Wayne State Physiology DepartmentSeminars; Detroit, MI, United States of America. 02/2024.
- Loss of SAS lncRNA triggers VSMC hypertrophy and cell cycle Arrest. III Encuentro Spanish Scientist in the USA (ECUSA); New York City, NY, United States of America. 10/2022.
- A Lnc(RNA) Between Epigenetics and Vascular Cell Function. ASIP Young Investigator Keynote Seminar Series; 06/2022.
- Loss of the smooth-muscle-cell-Angiotensin II-sensitive (SAS) lncRNA triggers VSMC hypertrophy and cell cycle arrest: Application to hypertension and aortic stiffness. Emerging Topics in Microcirculation Symposium at Experimental Biology2022; Philadelphia, PA, United States of America. 04/2022;
- Loss of the smooth-muscle-cell-Angiotensin II-sensitive (SAS) lncRNA triggers VSMC hypertrophy and cell cycle arrest: Application to hypertension and aortic stiffness. NAVBO Vascular Biology Annual Meeting. Online. 10/2021
- Loss of the smooth-muscle-cell-Angiotensin II-sensitive (SAS) lncRNA triggers VSMC hypertrophy and cell cycle arrest: Application to hypertension and aortic stiffness. PISA Young investigator virtual meeting 10/2021.
- Angiotensin-II-sensitive lncRNA controls VSMC hypertrophy and cell cycle. NAVBO Focus session on microRNA on vascular biology; 09/2021