My research focuses on understanding how transcriptional, epigenetic, metabolic, and RNA-regulatory mechanisms preserve cellular and vascular homeostasis and how their disruption contributes to cardiovascular, neurovascular, and age-related disease. A central theme of my work is the Kruppel-like factor (KLF) family of transcription factors, particularly KLF2, KLF4, and KLF15, which regulate cellular adaptation, metabolism, inflammation, and stress responses.
My research trajectory began during my doctoral training, where I investigated molecular mechanisms underlying brain injury and recovery following acute hypoxia. Using proteomic and molecular approaches, I identified epigenetic mechanisms associated with recovery and neurogenic responses, including regulation of KLF4. This work established my interest in how transcriptional and epigenetic programs promote cellular resilience following injury.
I subsequently joined Dr. Mukesh Jain’s laboratory at Case Western Reserve University, where my research expanded into metabolic and cardiovascular biology. My work on KLF15 investigated its role in metabolic flexibility and adaptation to energetic stress. Following the laboratory’s transition to Brown University, my research increasingly focused on endothelial and neurovascular biology. Our work demonstrated an important role for endothelial KLF4 in preserving blood-brain barrier and neurovascular integrity during aging, linking loss of endothelial homeostasis with vascular dysfunction, neuroinflammation, and cognitive impairment.
My current research extends these concepts to heart failure with preserved ejection fraction (HFpEF), with a particular focus on how endothelial KLF4 protects against microvascular dysfunction and pathological remodeling. I investigate how KLF4 deficiency alters chromatin accessibility and transcriptional programs and promotes inflammatory and fibrotic responses. By integrating genetically engineered models with single-cell RNA sequencing, spatial transcriptomics, chromatin profiling, and pharmacological approaches, I aim to identify mechanisms that can be leveraged to restore endothelial function in cardiovascular disease.
In parallel, I am investigating KLF2-dependent regulation of inflammatory and metabolic homeostasis in the context of aging and age-related disorders. An emerging direction of my research explores RNA modification and epitranscriptomic mechanisms that regulate inflammatory responses, providing an additional layer for understanding how transcriptional and post-transcriptional networks interact to maintain cellular homeostasis.
Together, my work is guided by a fundamental question: how do cells and tissues maintain resilience in the face of metabolic, inflammatory, and environmental stress, and how does failure of these adaptive mechanisms lead to disease? My long-term goal is to develop an interdisciplinary research program that integrates KLF biology with chromatin and RNA regulation to uncover mechanisms of vascular resilience and identify therapeutic strategies for cardiovascular, neurovascular, and age-related disease.
