Research
These are areas of research we are focused on, but also invite new collaborations and ideas which lead to new hypothesis-driven scientific knowledge and novel therapeutic development.
Heart Failure
Heart Failure (HF) is defined as a clinical syndrome in which the heart is unable to maintain cardiac output commensurate with the body's demand and is also one of the leading causes of death worldwide. The syndrome is classical described through changes in the left ventricular ejection fraction with various etiologies. Took account for heterogeneity of HF, we have preclinical models which recapitulate the major phenotypes of both HF with reduced (HFrEF) or preserved ejection fraction (HFpEF). We induce ischemic heart disease, various cardiomyopathies, or metabolically-driven perturbations leading to HF manifestation. We explore the mechanism(s) underlying the development and progression in hopes of identifying novel targets and therapeutic strategies to combat HF.
Gut-Host Interaction 
The gut microbiome and host interaction plays a critical role in overall health and well being. Modifiable risk factors, such as diet, smoking and exercise can alter this interaction and lead to changes in gut metabolites and the endocrinological profile. The shift in metabolites which have hormone-like properties lead to alterations in cellular signaling and physiological homeostasis. We investigate the underlying mechanism(s) in this relationship which lead to increase risk and severity of cardiovascular disease and explore novel therapeutic strategies.
CNS in Cardiometabolic Disease
There is a paucity of data understanding how sensory inputs from systemic organs (gut, liver, kidney and heart) into the central nervous system lead to changes in CNS outputs in a coordinated multi-organ response. This is never more true than for the CNS and cardiovascular systems. While classical physiological responses are well understood (i.e. baroreceptor reflex), there is limited comprehension as to how dietary composition (fats, sugars, etc...) and alterations in the gut microbiome, alters sensory inputs and reinforces, through dopaminergic excess, co-morbidities (i.e. obesity, diabetes, hypertension) and subsequent adverse CV outcomes. We are interested in understanding how gut microbial reorganisation and gut-derived metabolites alter somatosensory activation in the CNS leading to CV pathophysiology and cardio-metabolic disease (CMD). Also, understanding the mechanism(s) by which novel therapeutics alter these interactions.
Metabolic-Associated Steatotic Liver Disease
Metabolic-associated steatotic liver disease (MASLD), formerly known as non-alcoholic fatty liver disease (NAFLD), is a spectrum of liver disorders characterized by the accumulation of fat in the liver in the absence of significant alcohol consumption. MALSD is closely linked to metabolic dysfunction, including obesity, insulin resistance, type 2 diabetes, dyslipidemia, and hypertension, reflecting its systemic nature and association with cardiometabolic risk. The pathogenesis of MASLD is multifactorial, involving complex interactions between altered lipid metabolism, oxidative stress, gut microbiota dysbiosis, and chronic inflammation. Despite its rising global prevalence, there are currently no FDA- 
approved pharmacologic treatments, and management primarily focuses on lifestyle interventions targeting weight loss and metabolic control. MASLD also poses significant cardiovascular implications, as it is independently associated with increased risk of atherosclerosis and cardiovascular events—the leading cause of death in affected individuals. As such, MASLD represents a critical intersection between liver health and systemic metabolic disease, underscoring the need for integrated therapeutic strategies and early intervention especially in those who suffer with cardiometabolic disease.
Cardio-Renal Syndrome
Cardio-renal syndrome (CRS) is a complex, bidirectional disorder in which dysfunction in either the heart or the kidneys leads to progressive impairment of the other organ. This condition underscores the intricate physiological interplay between the cardiovascular and renal systems, driven by shared hemodynamic, neurohormonal, and inflammatory pathways. The pathophysiology of CRS involves a complex interplay of neurohormonal activation—particularly of the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system (SNS)—as well as hemodynamic disturbances, including venous congestion and reduced cardiac output. These are compounded by systemic inflammation, oxidative stress, endothelial dysfunction, and progressive fibrosis in both organs. The management of CRS remains challenging due to the difficulty in treating coexisting heart and kidney failure, and the lack of robust evidence-based therapies tailored to this syndrome. Given its high morbidity and mortality, CRS represents a significant clinical concern, requiring an integrated, multidisciplinary approach to care. We seek to understand the complex interplay through comics-based analysis in models of CRS.
Preclinical Translational Research
Preclinical research plays a critical role in bridging the gap between basic science and clinical application, offering a translational platform that closely mimics human anatomy, physiology, and disease progression. These models provide greater physiological relevance, particularly in fields like cardiovascular, renal, and metabolic research, where organ size, heart rate, and vascular architecture align more closely with human systems. These models allow for the use of clinical-grade imaging, surgical interventions, catheter-based techniques, and device testing, thereby enabling more accurate assessment of therapeutic efficacy and safety prior to human trials. Moreover, the ability to monitor longitudinal outcomes and perform invasive assessments in real time enhances the mechanistic understanding of disease processes and treatment responses. Despite their higher cost and resource intensity, these studies are invaluable for refining dosing strategies, optimizing delivery methods, and validating biomarkers or endpoints relevant to human disease. As such, we believe this research represents an essential step in the translational pipeline, ensuring that promising preclinical findings are robust, reproducible, and applicable to clinical settings. We have more than a decade of experience in developing and utilizing these preclinical models for interdisciplinary research in CT surgery, cardiovascular disease, gastrointestinal, pulmonary critical care and other fields.
Laboratory Collaborations
Lefer Laboratory - Cedars Sinai Medical Center
Brown Laboratory - Lerner Research Institute, Cleveland Clinic
Makarewich Laboratory - Cincinnati Children's Hospital