Sravan Perla, PhD, MSc

Research Background:

Sravan Perla earned his M.Sc. in Medical Biochemistry from JIPMER, Puducherry, India, before joining the Indian Institute of Science (IISc), Bangalore, where he conducted brief research under the mentorship of Raghavan Varadarajan (https://en.wikipedia.org/wiki/Raghavan_Varadarajan) and Upendra Nongthomba. He completed his Ph.D. at the University of Toledo and New York Medical College, New York, USA, under the mentorship of Ashok Kumar, Ph.D., FAHA, with doctoral research focused on the epigenetic regulation of the human angiotensinogen (AGT) gene. Following his doctorate, he joined Yale School of Medicine to work with Anton Bennett, Ph.D (https://medicine.yale.edu/profile/anton-bennett/), investigating SHP2 signaling in the regulation of heart disease, with findings published in high-impact journals including PNAS, JCI, and Neurology. He is currently working with Dr.Murat Günel MD, FACS, FAHA, FAANS (https://medicine.yale.edu/lab/gunel/profile/murat-gunel/) and Dr.Tanyeri Barak MD in the Department of Neurosurgery, transitioning from cardiovascular research to the study of brain aneurysms, where he investigates genetic profiling, advanced imaging, spatial transcriptomics, and cellular mechanisms to advance neurovascular therapeutic discovery.

Current Research:

My current research focuses on the role of PPIL4 in cerebrovascular development and integrity, with particular emphasis on its contribution to intracranial aneurysm susceptibility. Building on evidence that rare deleterious PPIL4 variants are enriched in individuals with intracranial aneurysms, I am interested in defining how PPIL4 dysfunction disrupts brain-specific angiogenesis, vascular morphology, and hemorrhage resistance.
At the mechanistic level, my work investigates the PPIL4–JMJD6–Wnt signaling axis. I aim to determine how PPIL4 binding to JMJD6 enhances Wnt signaling and how aneurysm-associated PPIL4 mutations impair this function, using molecular, biochemical, and cell-based approaches to connect altered protein function with vascular phenotypes.

Future Research:

My future research will define the cell-specific and developmental functions of PPIL4 in the neurovascular unit, including its roles in endothelial cells, mural cells, and vascular remodeling. I plan to combine functional studies of patient-associated variants with genetic disease models and vascular phenotyping to identify the signaling events that lead from impaired PPIL4-dependent Wnt activity to weakened cerebrovascular integrity and aneurysm formation. Ultimately, I aim to translate these mechanistic insights into strategies for improved risk stratification and therapeutic intervention in intracranial aneurysm. Identifying PPIL4-regulated pathways, biomarkers of vascular vulnerability, and potentially druggable nodes within Wnt signaling could help advance precision approaches for preventing aneurysm growth and rupture.

Our focus is to transform the fear and uncertainty surrounding brain aneurysms into hope. By developing new therapies that protect and strengthen the brain’s blood vessels, we aim to prevent devastating ruptures and give patients not only more time, but the chance to live safer, fuller, and happier lives with the people they love.