TACTIC: Endothelial Biology After Injury
- Project Focus: Mechanistic dissection of endothelial dysfunction as a central driver of trauma-associated coagulopathy and organ failure.
- This project investigates how acute injury and hemorrhagic shock disrupt endothelial integrity, glycocalyx structure, and vascular barrier function, leading to dysregulated coagulation, inflammation, and microvascular thrombosis.
- Using integrated in vivo trauma and hemorrhage models alongside human biospecimens, the work defines endothelial-derived mediators (e.g., adhesion molecules, extracellular vesicles, and inflammatory signaling pathways) that link vascular injury to platelet activation and coagulopathy.
- The goal is to identify endothelial-specific therapeutic targets and biomarkers that predict outcomes and inform biologically driven interventions to preserve vascular homeostasis after injury.
Nanomedicine for Hemorrhage Control: Translational Hemostatic Platforms
- Project Focus: Development and translational evaluation of synthetic and nanoscale therapies to restore hemostasis in severe bleeding.
- This project leverages platelet-mimetic nanotechnologies (e.g., synthoplates) and other novel hemostatic agents to augment clot formation when endogenous platelets or blood products are ineffective or unavailable.
- Studies focus on defining mechanisms of action, biodistribution, and safety in clinically relevant models of traumatic hemorrhage and coagulopathy, including settings of platelet dysfunction and dilutional coagulopathy.
- The overarching objective is to establish scalable, deployable nanomedicine strategies that complement or replace conventional transfusion therapies and can be rapidly translated to austere, prehospital, or resource-limited environments.
Mitochondrial Dysfunction After Injury and Post–COVID-19 Infection
- Project Focus: Role of mitochondrial injury in immune dysregulation, coagulopathy, and persistent organ dysfunction.
- This project examines how mitochondrial damage and bioenergetic failure contribute to endothelial activation, platelet dysfunction, and systemic inflammation following trauma and severe viral infection, including COVID-19.
- Using cellular, animal, and human translational models, the work interrogates mitochondrial DNA release, oxidative stress, and altered metabolic signaling as drivers of post-injury and post-infectious coagulopathy.
- The long-term goal is to identify mitochondrial-targeted therapeutic strategies that mitigate persistent vascular dysfunction and help explain prolonged thrombo-inflammatory phenotypes observed after severe injury and COVID-19.
My research program focuses on advancing the fundamental understanding of trauma-associated coagulopathy, with particular emphasis on platelet biology, endothelial function, and the molecular and cellular mechanisms that drive disordered hemostasis and vascular injury in critical illness. My work centers on defining how platelets, the endothelium, and circulating mediators interact to regulate clot formation, inflammation, and organ dysfunction following injury, hemorrhage, and shock. I pursue these questions through mechanistic and experimental studies that span in vitro systems and in vivo models, with the goal of identifying actionable biological targets. A major translational arm of my research is dedicated to the development and evaluation of nanomedicine-based strategies for bleeding control, including engineered and synthetic platelet-mimetic platforms designed to restore hemostatic function when conventional therapies are limited or unavailable. Together, this work aims to bridge discovery biology with innovative therapeutic approaches that can fundamentally improve the treatment of bleeding and coagulopathy in trauma and other high-risk clinical settings.